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"Test" for Autism Measuring Gut Microbes?

Gut-population-1233311 Read the full article in the UK's Telegraph. We ask the question, what is altering the "gut" microbes in these infants? And didn't a certain British doctor ask similar questions, relating autism with GI disease and lose his medical license? We hope this leads to more promising research into the brain/gut/autism connection.

Diagnosis of autism has always been difficult and often the condition remains unrecognised until too late for treatment to have a maximum effect.

But now researchers at Imperial College London have discovered a potential way of spotting the disorder in children as young as six months old.

That would mean that intensive behavioural and social treatment could begin before the disease has caused any permanent psychological damage.

Professor Jeremy Nicholson, the author of the study, said: "Children with autism have very unusual gut microbes which we can test for before the full blown symptoms of the disease come through.

"If that is the case then it might become a preventable disease." Read the full article in the UK's Telegraph.

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There will be a resolution someday for those with children with autism, but the highly unusual nature of the condition I have dealt with and the age of the person when I identified their problems means those in my circle will never understand no matter how much of what I have said is verified in autism. In 96 when I entered other autism boards to glean and share the clues of what was happening to cause all these problems I felt like an interloper trying grasp why we shared the same biological stories of problems, but my patient did not spin or hit their head. By far, this board and the plights that those here face are the ones I identify most with even though I don't have the typical experiences of those with affected children. I think I will end my sentiments and contributions here with the the best description of this condition. If you can contemplate an invisible inverted autism, you have the picture. I feel that the momentum towards all of this breaking the barriers of understanding and acceptance as regards to autism may have become unstoppable, and that is good.

Cheers to All.

Benedetta,

How is your situation? If you want to share what has happened I am interested.

Regarding Roundup, what I read suggests it has seen a lot of use since the early 80's and the glyphosate has been used in other agro-chemicals widely for qutie a whilde. This may still not be a time fram ewhich affects your family memebers, but Roundup or glyphosate clealry did not cause autism orginally as it was not formulated until 1971. However, it's increased use does overlap with the increase in autism to some degree and it could possibly contribute tto worse cases or be an exposure that pushes the relatively recent cases which may be in the sensitized group over the edge. This does not negate vacine causation, but may be part of setting more up for vaccine reactions.

Glyphosate Toxic & Roundup Worse

"Broad-spectrum herbicide glyphosate (N-(phosphonomethyl)glycine), commonly sold in the commercial formulation Roundup (Monsanto company, St. Louis, Missouri USA) has been frequently used both on crops and non-crops areas world wide since it was introduced in the 1970s. Roundup is a combination of glyphosate with other chemicals including a surfactant (detergent) polyoxyethyleneamine that enhance the spreading of the spray droplets on the leaves of plants. The use of Roundup has gone up especially in countries growing Roundup-tolerant GM crops created by Monsanto."

http://www.i-sis.org.uk/GTARW.php

Glyphosate

"1. Glyphosate was discovered by J.E. Franz in Monsanto Corp. in 1971 and released commercially in 1974.
2. In the early 1980's it became the first individual pesticide with world-wide sales of over $1 billion.
.....
1. Structurally, glyphosate resembles that of an amino acid. Specifically, it is reminiscent of phosphorylated glycine:"

http://www.agron.iastate.edu/~weeds/Ag317/manage/herbicide/ATgly.html

Phospholipid metabolism with Sphingosine and Lpa is possibly tied here, and Sphingosine and LPA are involved in either case.
interleukin-17 increases jeg-3 in certain placental cells increasing their number and involvement. This is also a proccess used in some cancer cells. If thise is latered in utero and set in stronger or has a longer than "normal" time frame of activation it could be the mechanism that induces the "invasive cancer like proccess" I suggested could be happeing in numerous cells in the cerbral cortex.

Benedetta,

I am sorry to hear of the medical emergency, I do hope all turns out well.

Nick

Nick;
Just thought of this one since you mentioned lipid metabolism in Kawasakis.
In one Kawasakis study it mentioned heat shocked proteins inside the mitrochondria.

Dr.Jon Poling (FDA neurologist - and won his case in the vaccine compensation case that claimed his daughter's mitrochondrial what ever was made worse by a vaccine) did mentioned in trying to explain what happened to his daughter that extreme temperatures may cause damage to some proteins inside the mitrochondria.

So I suppose he was thinking about heat shocked proteins - the same ones in Kawasakis.

Nick I have had a family medical emergency. It is not over with yet. I am just home for a few hours.

I read rapidly what you said.

Roundup has not been around long enough to the general population, to have caused anything with family .

Sure it is used a lot now, but only in the last decade has it really come into use.

This is a good step in the right direction as it is hopefully respected as sientific, but not news. Maybe it will facilitate more open minds about the immune aspect.

Autism study gives hope for cure

http://au.news.yahoo.com/thewest/a/-/breaking/10211083/autism-study-gives-hope-for-cure/

On second thought, leave tetracycline in that list along with tricyclics. If the strep bacteria is involved it may have a relation to tetracycline involment.

There are so many areas to look at that discussing one at any length requires that others have looked at enogh of the same areas to relate to what one might say about it's involment of distrubance and how it relates to other factors of biological function. Sometimes I intend to follow up a thought while coming to it in one area of study and I lose it from mind only to have it be triggered when studying some other area that also seems to relate. One such concept has come back and that is the idea that some property of disposable diapers is interacting with metabloites in the urine of kids exposed to these chemicals or already have a level of difficuly in immunity or metabolism and the products of the diaper reacting with the urine, and mavbe microorganisms, is acting like a compress for this byprouct and the genitals of boys might absorbing this more readily or the exposure is in an area more likely to create reactivity such as in the prostate or testes. I had briefly checked the connection at the time and had a component of the diaper in mind, but have forgotten what it was. I will have to go back and see if I can find what I felt it might be.

Benedetta,

In light of the tetanus shot problems you and your husband seem to have had I have a link to an Andy Griffeth show that will surely warm your heart. That is, iif you have the time and desire to watch iit all. You may have already seen it and had a visceral reaction. The defiant vaccine weary character does not come off looking well, but that is in the eye of the beholder. I am from the country and that must explain my ignorance.

It is called "The Country Nurse".

http://www.tvland.com/shows/andy-griffith-show/full-episodes/the-country-nurse

Another correction to the post 2 back. I did not mean tetracyclines. I meant Tricyclics as in antidepressants.

aromats = aromatase

I see the link to Roundup in ht news links on AoA and have been looking at it and glyphosate and glyceraldehyde 3-phosphate for while and the jaunt down the glycerol path a while back in our discussion puts this in a clearer picture as this chemical cacan be an endocrine disrupter and inhibits aromats. This would fit in with the problems I mentioned with my wife having trouble with aromatic compouns such as those in the drugs we have been discussing. This would tie int neurotransmitter functions as this enzme is invilved in tyrosine, tryptophan, and phenylalanine synthesis. I had looked deeply into this a few days ago although it had been on the suspect list for years. There is probably a synergy in the enviroment of elevations of many of many chemical compounds including azines like hydrazine, azo's, 2-Mercaptobenzothiazole, and those in tetracyclines and others. This would relate to epoxides, microsomal epoxide hydrolase,diacylglycerol, and a number of others.

Benedetta,

Yeah, DRESS is regarded as episodic and is another condition I considered when considering Kawasaki's, and Kawasaki's is determined to have a resolution or cessation of effects except for possible ongoing lipid metabolism changes. So, without my seeing the symptoms firsthand, and there being no report of "strawberry tongue" and a couple of other makrers for it missing I lean more towards a DRESS event in her. This is bolstered by the fact that I later discovered she had a reaction to Sulfa drug as a child. I am not sure what she was taking for it then, but it might have been at the time of the Scarlet Fever as a sulfa ,sulfadiazine, is given for it at times now. My thought is though that these conditions themselves are more manifestations of the problems already going on chronically in the individual and procceses that present with these conditions are going on to some degree like the tension in an earthquake. The effects are there and a trigger could relase a dmore destructive event and in these cases leave the people in chronic ill functioning conditions or elevate the process. This would be a triggered event in sensitized individuals or maybe be an event that elevates one from a mild sub acute problem to a chronic acute one like we propose vaccines may do as well. Again in some people it may be one of a few trigger events that are cumulative. The DRESS simply reveals a problem with the body being able to handle certain sunstances that are already involved in other metabolic and immune functions of the body. When a virus or drug is introduced the it goes ballistic. The actual event of DRESS and possibly Kawasaki's may be more like a reaction in the body to reset certain immune parameters either for better or worse. The list of drugs often setting off DRESS list athe bottom of the Wiki entry on DRESS Syndrome is tied to the chemicals drugs your family may has used, I know your husband has, and the list includes Carbamazepine and Sulfonamides like Bactrim DS that set my wife off. I relate this to phenylic sensitivity I mentioned in the notebook forward I linked to which ties back to Benz/phenol chemicals. This is almost certainly tied to the PST deficiency in kids with autism.

The drug list at WIKI is:


"Drugs that commonly induce DRESS syndrome include phenobarbitol, carbamazepine, phenytoin,[8] lamotrigine, minocycline,[9] sulfonamides, allopurinol,[10] modafinil and dapsone. It has been associated with HHV6"


That is what I was saying earlier when I wrote:

"The connection to the drugs with properties like Carbamazepine and their relation to metabolism and maybe immune dysfunction glows to my eyes."

There may well be a difference in certain aspects of biology and the causations and reactions in what disease states each affected individual manifests. It also may mean what helps or is problematic for each of our families may vary a bit. But, there are common denominators. Also, keeping in mind the reason we are at the this point in our discussion is the idea that a drug with properties like Carbamazepine can help cause spina bifia by inhibiting folic acid and the problems with compounds like these drugs may become intrinsic factors in disturbing metabolism and involve immunity related to them. As far your husband and his taking drugs with these properties after your children were born I would at least consider that it reflects some connection to a unusual relation to their properties in altering his system no matter how you look at it as it is not given to healthy people. In addition, while not a high possibility, the notion of Paradoxical dose effect might make it make more sense as to whether it was/is a metabolic issue in him as well effecting his immune system too.

I wanted to add now that I am back, that my husband also worked away from home a lot - almost constantly which also left me with a lot to do on the farm, the house, the kids plus I taught school.

Exercise maybe another thing that is important in all of this. The more you exercies the more mitrochondria is made. Of course there were times I was beyond going - I really could not - but when I could I did.

That is why I encourage and push the rest of my family to keep going, if they are interested in something I do my best to encourage their interest - except my son - his interest is video games so I have to make him a list of chores that has to be done every day.

Just one more treatment.

To get better it is a lot o

DRESS is were drugs cause a allergic reaction.
Steven Johnson is one - my son had that at one time with a epileptic drug call Lamitcal.
It is considered the Cadillac of the epilepsy drugs. It mellows their mood - not as in zommbies, but as in- it really works well. He had just come off of zonnegram (another epileptic drug) that made him evil, irritable, angry all the time,super depressed but really skinney and then on to Lamictal and oh it was nice.
And then one morning he took it and his neck turned really red, burned, and it did it again that evening too.

If he continued it - which we did not- it would have turned his skin to blisters, and slushed off - a very bad deal, ending him in the hospital. Some people have this from just taking antibiotics and they end up in burn units and treated like burn patients. Does not get any worse than that.

It is self limiting- stop the medicine and it goes away, unless it is so bad you end up in a burn unit or dead.

Sjögren's disease - three years ago they were for sure that my husband had it. It is an autoimmune disease of the salvitory glands. He went to a rheumatologist perpared to take quionine (the give this medicine to those with lupus too- anyway they even had his eyes checked before the next appointment becuase this drug can harm the eyes and they wanted a baseline on his eyes before starting this medicine) The ANAs are specific and although he had a lot of markers - it was not enough or complete enough for a dignosis of (sorjournes) the way I spell it because the is the way it is pronouced. But more things started happening at the time like he was not only having low oxygen as he slept but also as he sat in a chair and really low walking around. That has finally passed.

As far as a virus. Kent had me believing, but now I am very unsure. I too became very ill a few years back. but then again I had yet another tetanus shot that I forgot about after the one when I was 21 - another one - I might have been 35 or 36 or 40 I don't remember, and over the years I have had a slow but steady autoimmune diseae that took my hearing in one ear (it is fixed now with titanium steel), my thyroid, and then 45 I started having intense migraines, I was so tired I could not move but I got over it. I go all the time, I do man's work because my husband cannot and my son will not or can not - or maybe a little of both.
I don't know why I was able to turn it around but the Atkin's diet was not the beginning of me getting better, but I think it did stop the thyroid getting worse.

Got to go my husband wants me to drive him to town.

I can't help but note this unfortunate situation of Venus Williams. She has been diagnosed with Sjögren's syndrome.
I suspect I was transmitted a virus from my wife and had severe fatigus and all sorts of problems and had IBS and Pancreatits develop over times. The article on her mentions that she has also recently had a notable viral infection. This may have been a trigger of her autoimmunity or a symptom of immune deregulation maybe like some aspects of the virus related autoimmune conditions going on that some of us relate to autism. She certainly would get a lot of sun and so it could be Vitamin D related in her case. I think it would be good if she were aprised of the Marshall Protocol. Most likely she will be given steroids and other drugs that will likely worsen her condition over time.


Venus Williams pulls out of U.S. Open due to autoimmune disease

http://sports.yahoo.com/tennis/blog/busted_racquet/post/Venus-Williams-pulls-out-of-U-S-Open?urn=ten-wp2840

Benedetta,

I see you son's cholesterol is high too as you stated allready. It did not register the first time. It may be time for me to take another break. I am missing things and not considering things I should in looking at this, which is a sign for me to take a breath. I would proably do well to read more int he other threads as it seems they are often more social then technical.

I hate to hear of the mugging you are getting at the Kawasakis board. Don't give them the satisfaction of getting to you. Did you happen to look into the "DRESS" conditon I mentioned? Is Kawasaki's confirmed in you child?

Benedetta,

Between not being ablle to post and being a little abosrbed in thought I did not think of the intent of what you said. Sometimes things don't translate well in typed words. I am a bit releived to know you were joking. In that light it is good humor.

I knew D was made from cholseterol, but it did not enter my thinking as I was going down my trail. This fact does make sense in light of all this, and may fit into why D helps you guys and hurts my wife. This is back to what may be theexception in Marshall's approach or then again....?

Nick I was just playing on words, but yes I know the difference in Chromatin and Chromium . Sorry, just a poor joke and not a very good one either.

Chromatin had something to do with the first cloned sheep - not having a very long life because the chromatin threads were already short when it was born. I think that is right.

No, we have not tried biotin. I am drowning in vitamins right now. I am going to start this new taurine and I can't find the darn study, they are erasing things on the Kawasakis website to make me look like some kind of nut! Really that is probably not that hard to do. They have insulted me, been rude and now that they know I'll hang on like a leech, and still express my views, and apparently have a very thick skin they are doing something new. They put these things on a blog and the study on taurine from the NIH was one of them. Some one over there is really smart and knows a lot, even leading me to some good stuff (throwing me a bone) but it is a game with them and of course I am not smart enough to play it.
Sorry don't mean to rant.
But back to biotin; no, but I will look into it, I already have briefly and it looks promising.

Now back to the other stuff you have brought up. I am struggling to follow so give me a little time to catch up.

On the subject of cholesterol. Low cholesterol is more dangerous than high cholesterol when it comes to heart blockage, and heart attacks. I know this because a older, thin guy at church had this problem.

My husband had his initial reaction to a tetanus (dpt shot) at age 28. Shortly after his cholesterol sky rocketed. I thought high cholesterol was at least a middle age man's problem. We did everything we could to get it down. WE did not eat egg yolks for years. Then he had another reaction to another tetanus shot (stepped on a nail that went deep, required an operation to clean the bone and they scairt him into getting another).
Long story short a few years later he ended down at Emory clinic were they said he had acquired mitochondria cytopathy and it was dangerous for him to take statin drugs.
Well it is dangerous for him to have any thing that reduces his cholesterol - including the stuff that just absorbs it out of his stomach. A few months after taking that - he was not able to think, in pain and even after they took him off of it - he did not return to his full self.

It takes cholesterol to make vitamin D and vitamin D is nessacary for the immune system as well as other important functions. Not to have enough of it is bad and having too much in your blood to clog up your arteries is bad too.

But you know we finally got it down with the Atkin's diet eating all the egg yolks and butter he wanted???? !!!!!!

We just quite eating the carbs. White flour, white potatoes, and sugar.

My son is now 25, and last year he was found to have high cholestrol, but then he is no longer a little kid and his intial vaccine injury has been a long time ago-. I think that the metabolism is not able to absorb what is needed and is showing up in the blood because it cannot be absorbed. Have I told you this before? It seems like I have said this before if so I am sorry to repeat myself.

As far as the Carbamazepine he did not take this untill after our kids were born. But as far as his own health - I am sure this stuff is not good for him, but it is a rock and a hard place right now.
Die of a heart attack (he thinks) or the myclonic jerks could get worse too untill he has a grand mal seizure - they would probably try then to put him on Depokote and that really is a metabolism killer.

And as far as a simple answer; Maybe you are right and it will not be all that simple. It maybe will be lots of stuff that excites the immune system like pesticides, metals, bacteria changing their spots and morphing into something evil, and then vaccine antigen proteins themselves.

Benedetta,

Have you read all of my posts since the one “test 2”? The connection to the drugs with properties like Carbamazepine and their relation to metabolism and maybe immune dysfunction glows to my eyes. The fact that your husband has been on these types of drugs and they are possibly implicated in autism and other health conditions is My wife had such a severe reaction to Sulfa Drug that has some of these properties and the genes related to drug metabolism in the cell and NALP3 is hard to ignore, as NALP3 is also called “cold induced autoinflammatory syndrome 1”. This may also have something to do with the maternal antibodies that are being discusses in another thread and why children gestated during winter months are more likely to have autism. That is, if there is a correlation with cold weather during these pregnancies. Sometime after the TB meds my wife’s mother developed Reynaud’s which is a cold induced immune related disorder. Her mother’s father died of TB around 1940 and her mother was found to have a spot on her lung and was diagnosed with TB in 1957. She spent 3 months in the hospital and was on the 3 drugs I mention in a post sometime back for several months. In relation to strep one of the things she received with the other 2 drugs was Streptomycin. She was found to later only to be a carrier after treatment. Years later when tested the doctor said she must have really never had TB as it would still show even if she was only a carrier. I think that is much more likely that TB bacteria were still there, but in l-form and not detected by the test they used. My wife had chronic bronchitis and this could have been related to an l-form reversion to Mycoplasma Pneumoniae also finding expression due to her immune suppression/deregulation. The Strep may have also been affected in her mother at the time of the 3 drug regimen with the Streptomycin and in concert with he other drugs could have done something akin to what aspirin does in Reye syndrome and aspirin. These mycoplasma bacteria need ther sterol cholesterol to function and could reduce levels I theorize, and Step that may have persisted in Pleomorhic form produces Streptavidn which has a high affinity for Biotin. Biotin is involved in some metabolic orders like the ones implicated in our discussion involving carboxylation and the drugs we mentioned. While there is only a small amount of biotin delivered to the chromatin a shortage of biotin or more likely a autoimmune genesis or reaction in immune response to a protein linkage to this region could cause damage and cause ongoing release or cause chromatin damage passed on to offspring.. I will get to the cholesterol a little more at the end of this post.

If the cause does somehow turn out to be “simple” as you suggest it may be, the condition that it produces is anything but simple, and is very complex. For example, if it turns out a slight constant increase of cosmic radiation is the progenitor of changes in the population that changes the way in which all of the other factors affect biology you could say autism is “caused” ‘ultimately and in a way simply by increased cosmic radiation even if the cosmic radiation changes many environmental factors that lead to conditions that end up producing autism. The cosmic radiation as the simple cause may not even then suit everyone as some would wish to ask what caused the increase in cosmic radiation and whatever they found allowed for more exposure to it might be called the cause. This regression might be endless. While I can see a great amount of this basic system of connection and feedback I have not closed the loop and don’t know where what I see ultimately ends in connecting back to the mosaic of genes, chromatin, mutations, toxins, metals, drugs, bacteria, viruses, timing, and vaccines and to the matrix they can compose. Add to this that not all of the list of things I just mentioned need be involved in a particular case of autism and in the next one may be the trigger or the factor of greatest consequence means that if you are always looking for pictures of the development of the biology of different individuals with autism to look the same you will not come to the proper view of any. The likelihood that the there is a synergy of causation and that in different cases one of these factors may be of greatest consequence means that no one exact map of events unfolding in autism exists. But, there are common denominators. This model would predict that there is a mean of the total of pictures in which a certain picture sharing the same factors appears most often and looks more alike. If it is more environmentally caused or involved, than this is the mean picture at some level. The medical world has thought that the gene picture was the mean or even only picture up till now.
While strep may be pleomorphic it is not a mycoplasma. I am not clear on whether it’s pleomorphic properties are relevant to the way the some kid’s with Panda’s may be dealing with step, it is curious enough to warrant further study.

This was written when pleomrphism was thought to mean something somewhat different than today, but their observation is interesting.

“Collected Papers by the Staff of Saint Mary's Hospital, Mayo Clinic by Saint Marys Hospital (Rochester, Minn.) (1919)

"Mathers and Howell found a specific increase in opsonin in the serum of rabbits immunized with different strains of the pleomorphic streptococcus.”

http://www.lexic.us/definition-of/pleomorphic

I still have not written off a tie to the epidemic during World War 1.

SO-CALLED PLEOMORPHIC STREPTOCOCCI FROM HUMAN RESPIRATORY TRACT

Pleomorphism is not uncommon among bacteria. The classic example is the group of diphtheria bacilli. During the last few years a number of workers both in this country and abroad have noted the finding of streptococci in the nose and throat—particularly but not exclusively in influenza—having more or less varied morphologic characteristics. These have sometimes been designated as "diplostreptococci" and described as having flattened sides or as elongated, or they have shown a considerable variety of pleomorphism, with club-shaped organisms as well as elongated forms. Ribbert1 described such organisms during the influenza epidemic of 1889-1890. In the 1918 epidemic, Little, Garofalo and Williams,2 Averill, Young and Griffiths,3 Whittingham and Sims,4 and Donaldson 5 in England isolated pleomorphic streptococci. The latter investigator described a pleomorphic streptococcus which he designated as the "D" organism and suggested a possible connection between disease and the pleomorphic state. In the same”

http://jama.ama-assn.org/content/76/15/1003.short

Osteopontin functions as an opsonin and facilitates phagocytosis by macrophages of hydroxyapatite-coated microspheres: implications for bone wound healing.
“Osteopontin (OPN) is a secreted protein abundant in mineralized tissue extracellular matrices and bodily fluids. Previously we have shown that mineralized debris at surgical wound sites in bone and teeth are coated by macrophage-derived OPN and phagocytosed. Here, we have performed opsonophagocytosis assays to determine whether OPN acts as an opsonin and facilitates phagocytosis by macrophages of protein- and hydroxyapatite mineral-coated microspheres. Moreover, we have examined the opsonization effects of monomer OPN versus OPN polymerized (crosslinked) by tissue transglutaminase 2. Murine macrophages J774A.1 were exposed to polystyrene-latex microspheres having different surface chemistries (non-ionic, aldehyde amidine, carboxyl and aliphatic amine) which were coated with either serum albumin, immunoglobulin, monomer OPN or polymer OPN. Similar experiments with the same protein coatings were performed using hydroxyapatite-covered microspheres. Internalization of microspheres by phagocytosis into macrophages was confirmed by co-localization with the (phago)lysosomal markers lysosome-associated membrane protein-1 (Lamp-1) and LysoTracker, and by light microscopy and transmission electron microscopy after serial sectioning of plastic/resin-embedded cells containing microspheres. OPN significantly increased phagocytosis of both microspheres and hydroxyapatite-covered microspheres compared to negative controls (albumin-coated and uncoated microspheres), with phagocytic indices similar to, or greater than, those of the positive control (IgG-coated). The effect of OPN and hydroxyapatite on microsphere phagocytosis was synergistic. Polymer OPN further enhanced the phagocytosis of aliphatic amine and aldehyde amidine microspheres. Taken together, these results indicate that OPN is an effective opsonin able to facilitate particle uptake (including mineralized particles) by macrophage"s.”

http://www.ncbi.nlm.nih.gov/pubmed/18656563

You mentioned cholesterol, and since my wife has in the past had fairly low levels and it seems to tie to autism in some others I have tried to get an understanding of what the connection is. Lipid metabolism at some point surely is connected, but trying to see where it fits in the chain of events or how much it is a contributive cause or a symptom or both {most likely} is difficult. It does seem to have a possible relationship to mycoplasma bacteria, maybe specifically Mycoplasma pneumoniae.

Wiki

“Mycoplasma pneumoniae is a very small bacterium in the class Mollicutes. It causes the disease mycoplasma pneumonia, a form of atypical bacterial pneumonia, and is related to cold agglutinin disease...... This species lacks a peptidoglycan cell wall, like all Mollicutes. Instead, it has a cell membrane that incorporates sterol compounds, similar to eukaryotic cells.”

Wiki Mycoplasma

Mycoplasma refers to a genus of bacteria that lack a cell wall.[1] Without a cell wall, they are unaffected by many common antibiotics such as penicillin or other beta-lactam antibiotics that target cell wall synthesis. They can be parasitic or saprotrophic. Several species are pathogenic in humans, including M. pneumoniae, which is an important cause of atypical pneumonia and other respiratory disorders, ... Cholesterol is required for the growth of species of the genus Mycoplasma as well as certain other genera of mollicutes. Their optimum growth temperature is often the temperature of their host if warmbodied (e. g. 37° C in humans) or ambient temperature if the host is unable to regulate its own internal temperature. Analysis of 16S ribosomal RNA sequences as well as gene content strongly suggest that the mollicutes, including the mycoplasmas, are closely related to either the Lactobacillus or the Clostridium branch of the phylogenetic tree (Firmicutes sensu stricto).

So, when taken together you see that the M Pneumoniae is tied to cold agglutenin disease

Since my wife had low cholesterol and frequents bouts of bronchitis.

I had posted this blurb on another site that was discussing Jenny McCarthy and biomed.

New study shows low cholesterol levels could have negative effect on autism

"Today Rose is reading, smiling, and interacting like never before. And a packet of cholesterol could have helped make the difference.
As part of a clinical trial, the Barkers added a packet of cholesterol to Rose's diet twice a day and that simple act may have had a profound effect.
Dr. Eugene Arnold with Ohio State University Medical Center says, "It's possible that too low cholesterol could be one of several causes of autism, affecting a sub-group of children with autism."
Dr. Arnold launched an initial study with a simple premise. Knowing that proper levels of cholesterol are essential for brain development and function, he wanted to see if increasing cholesterol could reduce symptoms in autism."
If her cholesterol level is relevant to her autism, I wonder why her levels were low?

http://www.abc2news.com/dpp/news/health/childrens_health/new-study-shows-low-cholesterol-levels-could-have-negative-effect-on-autism

The next article is about genetic defect in cholesterol metabolism, but it may inform what altered cholesterol levels may affect.

Research Demonstrates Immune System Connection to Low-Cholesterol Syndrome

"Juan Rivera, Ph.D., director of the NIAMS Office of Science and Technology and chief of the Molecular Inflammation Section, became interested in SLOS because his lab had been studying a type of inflammatory cell called a mast cell, the principal cell in triggering allergies, including food intolerances. In previous studies, his group had found that cholesterol is a key component in mast cells' ability to initiate signals that tell other inflammatory cells to either rev up or slow down. "We made the hypothesis that one of the issues related to the food intolerance is that these mast cells are somewhat more hyper-responsive in these individuals and that led them to being easily triggered," he says."

http://www.niams.nih.gov/News_and_Events/Spotlight_on_Research/2006/low_cholesterol_syndrome.asp

Benedetta,

Have you ever tried high doses of Biotin for your family?

Benedetta,

Chromatin is not a a metal. It is something I posted an article about and how enviromental stress can affect chromatin/dna and affect gene expression a while back and have alluded to a few times since. I suggested that the "pink disease" grandparents may have had these effects in them and passed them on causing a greater risk of autism in their descendants as their gandchildren have 7 times increased incidence. I also, theorized that the increased vaccinces of the last generation might be what interacts with those descendants that causes this to become a greater problem. Other "stressors" could possibly lead to this as well apparently. But, a lot of our lconverstion of late is surrounding what the stressors may be or what is hindering the metabolism in those whose system may already be function may be operation under the condition caused by this chromatin produced stress condition.

Wiki - Chromatin

"Chromatin is the combination of DNA and proteins that make up the contents of the nucleus of a cell. The primary functions of chromatin are; to package DNA into a smaller volume to fit in the cell, to strengthen the DNA to allow mitosis and meiosis and prevent DNA damage, and to control gene expression and DNA replication."

http://en.wikipedia.org/wiki/Chromatin

Nick;
I hope your daughter starts feeling better, as well as all of your family.

Pain in the spleen, high up on the left? Sometimes that is hard to distinguish from the stomach. Thyroid it seems to be so very delicate and so very linked to all of this.

Carbamazepine is a dibenzazepine my husband has been on one of these since he was 35. Panic attacks after his immune system was destoyed by yet another tetanus shot (probably aka DPT shot). He recently developed myclonic jerks and they took him off of the xanax and put him on clodopine (spelling is way off) but it is just another dibenzapine as is xanax.

You spoke of Chromatin but what is causing problems on any of this.
Chromatin sounds a lot like Chromium a metal found in pigments of paint - yellows, reds and black.

So we now have in easy reach three heavy metals; chromium, mercury and aluminium.
Of course our immune system can't handle the microbes like it is suppose to, it can't even metabolizes the sugars anymore.

Here is a new supplement I have recently ordered and hope againest hope that is will help. I found it on the Kawasakis website - which by the way they say the long term prognosis is a messed up lipid metabolism. They say that means low cholesterol at first and then later high cholesterol - I think though that lipid metabolism is just another way to say acquired mitrochondrial cytopathy.
oh the supplement is Taurine. I was looking for the study but could not find it. I will go now and look some more.

With the last description of typical found microrganisms in the body it may be helpful to thinking about their pupose in human existence and health. As opposesed to higher organisms microorgansisms are like water and simply respond to their enviroment. I don't think we concvieve of them as having designs on conquering or of having some directed goal except to exist as their current state of enviroment and adaptation precipitates. Like water many will fill voids and repond under pressures and even change form depending on the conditions, but don't intend to promote or deystroy human health or arrive at a certain condition of their own except to meet the conditions of their enviroment that must always include their survival. Therefore asaults they are unconditioned for cause them to respond in a way that upsets their normally benign presence in the body.
This view means that even the l-forms blocking of the VDR is not something they undertake to evade destruction although that is the effect, but an action they always attempt to mediate in a typical functioning body that is normally producing countering actions that are normal and beneficilal to the host and therefore to all its inhabitants in healthful conditions that they have been conditioned to. They are the reason we have a VDR as it is.

Since I accidentally brought up Pleomorphic bacteria I want to make a clarification. I am not sure the case is totally closed on extreme pleomrphism, butit is likly not going anywhere to build any ideas on the notion that it occurs. Pleomrphic bacteria, on the other hand, are quite relevant, but I meant to avoid to term as it can evoke a response that it is bogus as extreme pleomrphism is widely rejected. A cell wall defiecient form or also a pleomorphic form of a cocc ilike streptococci and of other bacteria like clostridia, lysteria, and helicobacter pylori are relevant in the bactreial component of immune interaction and chronic disease.

If a strep can change form into a almost undetectable form then it may be that the treatment of it in some children developing autism may cause them to be part of the progression of causation or intensification of immune mediated autism. This may explain the expression of "pandas" in autism as waxing and wwaning. The H Pyloria could be doing the same. While Marshall did not discover L-form bacteria, as it was discovered I think in the 1930's, I crefer to them as the Marshall bacteria as he is the one who has suggested their route of disease causatrion and how to treat for their pathology.

One thing that I don't know if he has talked about is thier typical place in human biology. In the gut it seems generally accepted that their is a general balance of bacterial populations that are present in a relatively healthy biology. Though the populations will vary in different populations and still are reflective of a functional microbiome. So, no one mix of gut bacteria is a marker of a healthy gut population. It seems reasonable that l-form bacteria would also be present early on in a persons life as the gut is also colonized early in life. If their is a proper degree of peace or war between the viral, bacterial, and fungal populations and the human immune system than there will be a larger degree of health in such a person. This would be a homeostasis of expected microrganism interaction with the immune system and chemistry. Anti-biotics, metals, steroids, diet, and other factors can interfere with the homeostasis and some will tolerate alterations better than others. In the case of H Pylori it is noted that they are found to be the biggest cause of ulcers in the stomach. Yet, it is also suggested that they are normal flora in humans and may play a role in health. So, it may be that since in the gut there is a proper balance of immune interaction and populations of certain bacteria that reflect healthy gut function there may be a proper level of l-form bacteriaal strains in the body that begin to function pathogenically when the immune system is altered, or dysbiosis occurs in the gut, or toxins and metals are in one's system. Other factors could alter this balance as well. Genetic, Chromatin effects could set the stage for an altered chemistry and immune stae mediating the bacterial pathogenic state or one of the other factors including vaccines may be the trigger, especially in the sensitized individual.

Correction

In the last post I meant to put Mycoplasma bacteria, not pleimorphic bacteria.

Benedetta,

This was to be part of my Saturday post relating the concerns about my daughter. The l-form /pleimorphic bacteria are of interest here.

I found this after writing the earlier comment on my daughter’s spleen area pain and it makes me more concerned about my suspicion.

Rare Immune Cell Is Asset and Liability in Fighting Infection

“In papers published online in Immunity, scientists at Washington University School of Medicine in St. Louis reveal that the cells, known as CD8 alpha+ dendritic cells (CD8a+ DCs), can help the body beat back infection by a common parasite, but the same cells can be hijacked by a bacterium to decimate the body's defenses.”

http://www.sciencedaily.com/releases/2011/08/110826192436.htm

Also, this was up today and it is old news, but a step towards showing the relation of gut dysbiosis in chronic disease as we have seen in Autism cases and other autoimmune conditions.

Eradicating Dangerous Bacteria May Cause Permanent Harm

“Dr. Blaser sounded the alarm to the medical community and to the general public, that the widespread use of antibiotics may be having unintended consequences causing permanent changes in the body's protective, friendly flora and causing harm to the body's natural defense system. This may be even more dangerous to health than the creation of resistant "superbugs," which have garnered much attention over the last few years.”

http://www.sciencedaily.com/releases/2011/08/110824131547.htm

In an attempt to get something posted I left out part of what I wanted to add to the last post on Carbamazeapine. It is actually the article I alluded to and said go to the link below.

New Model Predicts Environmental Effect of Pharmaceutical Products

"Sometimes, some substrates can even revert to the original drug within the water treatment plant itself, increasing the concentration of the drug in the effluent discharged, as is the case with carbamazepine (a psychotropic anti-epilepsy drug)," says Xavier Domenech, co-author of the study and a researcher at the Department of Chemistry of the UAB.
The result is that a great variety of drugs that could be harmful to wildlife end up in the environment. "This is of greater concern in the case of water treated for human consumption, in which we are increasingly detecting a cocktail of drugs at low concentrations (nanograms per litre), the long-term effect of which is unknown," explains Domenech."

http://www.sciencedaily.com/releases/2011/07/110728082302.htm

Benedetta,

I have had trouble posting this since Saturday.

I have long ago considered Kawasaki’s in her, but felt a holistic approach would deal with this if it were part of the problems and never sought testing directly for this. But, she did not display most of the symptoms of the condition and from what I remember from back then her mother did not recall the “Strawberry tongue” or other signs of it, though I have read it can have effects that do not include some of the more typical markers. It is only a lesser part of the problem either way and I don’t think she had/has it. She has/had low thyroid and antibodies to thyroid, but the Marshall Protocol has helped in negating her need for thyroid medication. My son had a fairly high anti -thyroid antibody level, but we have not taken any steps with him as he is relatively ok at this point, but I do keep a close eye on his health indicators. My daughter has not been tested as she is 5 years younger than he and did not show any markers at the time of testing of her mother and brother. She is showing some signs of problems now and I am making an appointment to see the doctor about getting her on the Marshall Protocol. She is showing an indication for possible osteoporotic conditions and has been having intermittent pains in the area of her spleen. She has a few other markers as well.

It is interesting that Spina Bifida has entered our conversation in light of folic acid needs and the environmental influences involved in causation. Also, in light of my mentioning of benzene and phenol related chemicals in a post not too long ago as being involved along with carboxylation problems and the synergies of affect of environmental factors and the fact that folic acid supplementation before pregnancy is thought to reduce the incidence of Autism.

Here is a link to an article referring to a chemical being considered from a drug metabolite that ends up possibly in the water. This could be ingested in public water consumption. The drug is Carbamazepine and this is just one drug that they are looking at. Think of how many others could do the same or are having effects on biology when taken as medications.

Wiki – Carbamazepine The whole Wiki entry on this drug is worthwhile.

Go to the link on this drug and read the relationship to Depakote and a number of other drugs and its effect on CYP450 and drug metabolism. Intrauterine exposure is associated with Spina Bifida. Note the effect on mEH, this appears to be a key in these problems. The TB drugs I mentioned my wife’s mother took probably did similar things. The tie to anti-depressants and certain benzoic compounds is strong.

There appears to be a lot of linkage to mEH and a condition called DRESS, but there are many other genes and pathways involved or affected. Instead of Kawasaki’s the issues may be/have been DRESS related to drugs/chemicals and subsequent or co-occurring viral involvement and immune reactions pre-post natal and in utero and dysrgulating immune ability to deal with bacteria. If it is Dress related, drugs given for Scarlet Fevet and related infections could be the actual offender or be the additive factor to the strep causing the dysfunctional aspects of this contributor. The altered suppresion and metabolic factors after infection and drugs could be leaving a latent infection we call "Pandas" and their waxing and waning is noted by parents in their kids. My wife will occassionaly have moderate inflamation in her tonsil region with more swelling than pain. This has beeen disappearing on the Olmesartan as has her bone spur pain.

Carbamazepine = 5H-dibenzo[b,f]azepine-5-carboxamide"

http://en.wikipedia.org/wiki/Carbamazepine

Test 2

small edit to last post

"but a step towards showing the relation of gut dysbiosis in chronic disease"

Test

Nick;
Your wife having scarlet fever as a child.
It could have been Kawasakis.
It is rather hard to tell them apart.

How are your children?

Benedetta,
Well, you don't hear about it, but I think the biggest reason we don't is not because it is gone. If my sources are accurate the peak amount of Spina Bifida was about 3,000 live births a year in the U.S. . It is about half that number now, maybe a little less and this has been due to folic acid as you mentioned. There are other childhood conditions that eclipse this figure and the shifting away of focus on a condition with low annual numbers is something that would be expected especially when there is a notable decline in cases. A more notable reason for the shift away of focus I think is Autism, and to a lesser degree ADHD, which has/have become the prominent childhood condition{s} getting attention and there are tons more cases of Autism each year now, and for a number of years now, than Spin Bifida and more Autism now by far than Spina Bifida annual rates at their peak.

Oh I should add that although Spina Bifida is still around a lot of different drugs do cause it too, probably by reducing folic acid in the mother at the critical time it is needed.

Depakote for one.

So who knows what these women were taking in the 80's and then was quietly done away with or taken out of some medicine. Because incidents of Spina bifida has gone down

Benedetta,

I wrote:
"If you have not read what I wrote about it years ago you could go to the site linked below and read post#17."

I was incorrect. It is post 12 and they are not numbered, so you have to count down. There are 17 comments in the thread and somehow it stuck in my head that mine was #17.


http://autism.about.com/b/2009/07/27/kids-with-autism-have-no-special-gi-issues-debate.htm


Benedetta,
Well, you don't hear about it, but I think the biggest reason we don't is not because it is gone. If my sources are accurate the peak amount of Spina Bifida was about 3,000 live births a year in the U.S. . It is about half that number now, maybe a little less and this has been due to folic acid as you mentioned. There are other childhood conditions that eclipse this figure and the shifting away of focus on a condition with low annual numbers is something that would be expected especially when there is a notable decline in cases. A more notable reason for the shift away of focus I think is Autism, and to a lesser degree ADHD, has become the prominent childhood condition{s} getting attention and there are tons more cases of Autism each year now, and for a number of years now, than Spin Bifida and more Autism now by far than Spina Bifida annual rates at their peak.


Well yes, that too, Nick, but there was a special push for spina bifida in the 80's.
And the public did have problems with mixing up the two, so they distinguished the two by saying Jerry's kids and then there was spina bifada. Spina bifada is whimiscal enough name people could remember it. Still when they had the cute kids on the postures they always had in big letter: Spina bifida to help separate the two. There was at one time more effort to try to get people to pay attention to spina bifida than Muscular dystropy, believe it or not!
At the time I was carrying my second child there was a 5 year old in my daughter's children's group at church. Plus I knew of several others around in the community that I also know personally. So, there were a lot of them popping up in the population and nobody had a clue. It was of course genetic was the first thought in everyone's mind.
The OBY told me as I was expecting my second child that at last they had a test to check and see - I like everyone else just assumed it was genetic and they were testing DNA - which was very naive of me. I don't know what they were testing for to see. But you see how it was complicated when it was all so simple. It would never help those kids already born and for them I am so sorry. The five year old girl at church could have been a posture child. She looked just like her mother pale transluent skin, that really set off their black wavy hair and black eyes. But it stopped the growing epidemic - you don't hear anything about this disease now do you?


Benedetta,

"Have you been around long enough to remember all the postures of cute little kids incased in leg wrappings and standing with the help of crutches?"

I remember the kids on crutches having I think Muscular Dystrophy. Is that what you are reffering to? There were little donation sets with these kids with crutches in all the stores. I remember that very well.

Benedetta,

While your point is valid the same can be said about every disease for which no cause or prevention has yet been found. Since, I don't have a definitive answer I can't say that it is not one thing and that the cause would seem simple if it turns out to be one easily addressable thing. I did say though that it could be one factor that lights the fuse, but if Autism is a predominantly modern condition I don't think it is caused mainly by a low level of a particular vitamin. If it is vitamin related it is likely something in the modern environment causing a deficiency and that is not quite simple in itself. I seriously doubt it is simple in Autism though, I would be shocked if it turns out to be the case. Even in spina bifida there is an underlying predisposition as pre-pregnancy folate is only believed to reduce occurrence by around 70%. In spina bifida there is a specific neural tube defect and in Autism there are what appear to be multiple problems in many cases and this suggests a more complex set of conditions leading to Autism. I must admit I think am old enough to have been around when it was more common, but did not pay that much attention to a lot of conditions outside of mental retardation and cancer until I was an adult.

I do wonder what the rate of Autism would be if there had been no exposure to mercury in anyone in the last 100 years, or how much lower if no Alum had ever been put in vaccines. Even with mercury you have to ask with all the mercury used in treatment for disease dating back long before Thimerosol why wasn't there Autism being brought about from its use? The sense I get from all the information produced about Autism leads me to what I have laid out in the recent post, but it would be easier if you are correct and it is one simple thing. This does not address the Autism that is stated to be caused by genes alone it seems, as in Fragile X. The authorities suggest genetic causes alone may account for up 15% of known cases, but I don’t think there number is written in stone. If it turns out to mercury from many sources it might prove a challenge to reduce environmental mercury sufficiently or find ways to counteract its effect in the body to stop the dysfunction it may be causing leading to Autism. Until a simple or complex answer is found I will keep digging, though I do think I have a somewhat complete picture of my wife's arrival at her condition. Though she was never diagnosed I find her to have a form of Autism, but with other biological problems that distinguish her condition. If you have not read what I wrote about it years ago you could go to the site linked below and read post#17. While I say edited since a certain date at points in that posting, the only changes made were grammar and spelling corrections. It probably could use more of those.

http://autism.about.com/b/2009/07/27/kids-with-autism-have-no-special-gi-issues-debate.htm

Could be Nick,
or we are making it to complicated because we have not figured it out yet.
Example spinda bifida was merely a lack of folic acid at a certian time in the fetus development. Have you been around long enough to remember all the postures of cute little kids incased in leg wrappings and standing with the help of crutches?

I also remember when the egg shells of ball eagles were breaking and they could not figure it out. Some scientists thought the adult birds got too excited about the first one hatching and were cracking open the rest will celebrating. Then finally someone started measuring the strength of the egg shells.

I also remember the Ebola virus - it was nothing more than a virus in bats and it all started and spread from eating bats.

Children of the Aboriginals in Australia really were dropping like flies from vaccines and all they did was add vitimin C.

It is going to be simple when we find the answer, - if they were really trying to find the answer, and when they do people will be saying - now why couldn't you have found that answer sooner?

Benedetta,

You wrote:
"Kent Heckenlively one of the writers here on this web site thinks it is the XMRV virus.
Dan Olmstead and Mark Blaxill think it is mercury.
There are some that think their kids were not able to fight off the measles vaccine's half dead virus because well lots of theories there too.."

This is part of the problem and in some cases each may be correct. It is the chicken and the egg problem. The probability that different factors are involved at different stages in different children means that not only could one factor be the fuse in one case and a different factor the fuse in another it may be a synergy that starts things off in another. I think that when one factor is the fuse and the process begins it allow others to become a problem and elevates it into a much greater system wide problem. This is why I spend a bit more time on susceptibility. I think mercury can be a fuse, a virus, or Alum, and even at times the vaccine antigen is a fuse in the gut. In every case it leads to a syndrome when it is a biomedical related Autism case. That is it ends up affecting many systems in the body. If Autism has only been around in any noticeable form for maybe the last 70 years and is increasing, what is causing the susceptibility? Vaccines do not cause Autism in everyone though they may well be causing immune related problems and contributing to or causing disease in a great deal more. Is it simply the chronic increase in chemicals, drugs, pollutants, vaccines, and viruses arising from a changed environment or from lab creation being too much for people with certain genetic profiles or in some exposed to a certain virus? Or, are their prime factors like mercury {the pink disease, thimerosol, amalgams and mercury pollution mainly predisposing or causing the effects? Maybe increased benzene altering bacterial populations in humans. Or, is it the stress effects in an parents messing with the genes in ways we have discussed causing sensitivity and the other elements too much for such altered genetics? Is Marshall correct that the bacteria are being turned up by environmental effects like steroids and certain anit-biotics and they are the cause? Or is it some combination for different subsets? We may have to ready to accept it can vary in etiology. One thing seems clear to me something is different in the human environment and exposure in the last 100 years that is causing most of the Autism and certain aggravating factors have been introduced in the last 2o-25 years. This shifts suspicion a little more to vaccines and viruses for the aggravating factors in the last 20-25 years.

Add to this that many say there is not Autism, but many Autisms and the recipes leading to Autism might make a very large cookbook. Yet, the fact that so many parents report many of the very same health symptoms, behavioral profiles, and problems with milk and wheat suggests that there is still a unifying vein to the causation generally and this vein is best distinguished by issues with immunity and inflammation.
Using an analogy of disease states being like a huge lock with a great number of tumblers may help see the problem of human disease and Autism. For this analogy consider relative health as a key that won’t even go in the lock and that when it does it may begin to unlock certain disease conditions and that the key and lock change a bit over time. When a key opens a lock it has to be able to contact all of the tumblers correctly and in the right timing sequence. If it is a disease unlocking key it can align the tumblers of the lock that releases certain diseases or malfunctions. This is a positive action when we want to unlock a door, but in this analogy it activates disease. In our lock certain tumblers must be hit properly before other tumblers can be hit properly. This would be a like the order for unlocking a particular disease releasing processes. When certain tumblers are hit certain diseases may be an expression of this event at different ages of development and may only contact a number of tumblers, but not all and certain tumbler activation numbers produce more severe Autism. In Autism the key hits certain tumblers very early in life. If these same tumblers were hit later in life a different presentation of the effect would be seen as the key and lock changes through time. The key is all exogenous factors and the lock or all intrinsic biological factors. If enough tumblers are hit you die unlocking fatality in disease. This would suggest that those with biomedical involved Autism will have shortened life expectancy, if not arrested, like many diseases predict.

Yes Nick, I agree, more reading and thinking and talking with my husband. So don't worry about it for now.
Thanks

Nick;
The first time I had a yeast infection was when I was 21.
I was a newly wed, and a new job that required a tetanus shot - it developed about a couple of weeks after the tetanus shot. I did not even think of the tetanus shot at that time.

I had another tetanus shot years later - maybe 38 or so (I can't remember) I noticed nothing except my spring allergies became worse, and I slowly lost all of my hearing out of my right ear. It had calcium build up on one of those three little bones in the ear. I had it replaced with titamium steel wire. How much inflammation was caused by the operation itself let alone titaium steel, I don't know; but I am glad to have my hearing back and would pay that price. I also slowly lost thyroid function. Not a little thyroid function but a lot. I am on a pretty large dose of thyroid medicine.

I did not even think of this last tetanus shot as the beginning of my really minor health problems, compared to others, but now I do. Right now, I am fine - I go all the time except when I blog.


It may very well be that no one gets aways without any reaction to vaccines, but it so slow in development for most they do not blame the vaccines.

For those that have more acute reactions, fast reaction,- everyone is wondering here on this site, why. Marshall is a very interesting read and it could well be a bacteria. It sure took medicine long enough to realize ulcers were a product of a bacteria, or legionaire's disease, or even lyme disase. Kent Heckenlively one of the writers here on this web site thinks it is the XMRV virus.
Dan Olmstead and Mark Blaxill thinks it is mercury.
There are some that think their kids were not able to fight off the measles vaccine's half dead virus because well lots of theories there too - except I noticed that Cedillo (the family that went all the way the supreme court after losing in the vaccine court) blamed the DPT shot setting up their child to react to the MMR shot.
Aluminium is certianly no innocent metal to be injected into your body even if it is safe to drink a pop from.
Then there is the protein from the dead bacteria in the vaccine. Tetanus and pertussin are both proteins not from the dead bacteria but from the toxin these two bacteria produced.
I am sorry to bore you, you know more than I do on all of this- you are into metabolic pathways that I can barely follow.

Benedetta,

"We live a couple of hours away from Louisville now.
So Louisville is not too far."

You may need time to read and think about if the Marshall Protocol is something you want to try. But again I will mention, I can provide contact information if decide you want to see the doctor in Louiville.

Oh, the Candida symptoms also included a coated tongue with a white cast, chronic sore throats, and ongoing low grade fevers. At times my feet would be somewhat swollen in the morning, my hands also felt swollen and stiff alot, and I woke up feeling like I had been on a bender. When I think back on it it was hell.

Benedetta,

This is interesting. The worst "die off" problems my wife has ever had were from dealing with yeast overgrowth back in 96. She had been carrying this problem for possibly most of her life. A lot of parents talk about the yeast problems in their kids. The carbs, especially simple carbs, are the source of fuel for Candida yeast. I also started having yeast problems after getting married. To be blunt, I started getting many symptoms like severe anal itching that was temporarily helped by topical hydrogen peroxide, urinary tract problems, severe itching in my ears , , a lot of gas and stomach issues, pain when moving my eyes in any direction other than straight ahead, sunlight caused pain in my eyes, nose bleeds, some blood and unusual mucous in stool, increased allergies, sinus congestion and drainage, very puffy eyes with dark areas and at time creases under my eyes as though very tired. This symptoms subsided through yeast treatments though the die off was bad and I had bad headaches and the rubber band effect around my head and white cream formed in tear duct area of my eyes especially in the morning during the die off. I suspect I too carry the Marshall bacteria and was susceptible to their development after exposure to the bacteria and yeast after getting married. In other words my wife exposed me too this. I think I was in a weakened state immune wise as I had a lot of mercury put in my mouth in the fifth grade and a year later had severe strep that required penicillin to subdue. A year later blood was found in my urine and from that I was found to have some glomerulonephritis. The reason I suspect viruses play a decent role in elevating these problems is that no very long after my first encounters, at length, of kissing my later to be wife I became terribly exhausted. This may sound like mono, but it did not go totally away and would episodically zap me for some periods of time and this went on for years. The yeast treatment greatly reduced the fatigue amount and frequency of occurrence.

So, when you talk of how bad you felt beginning a low carb diet it makes me think you were having yeast die off. The bacterial die off has some similarities, but would probably not happen that severely from carb restriction alone. I am not sure of this though. I don’t think you would have to have female yeast problems for the yeast in your gut to be a problem, but it would be much more likely.

Nick;
We use to live in Bardstown only 40 minutes away from Louisville.
We live a couple of hours away from Louisville now.
So Louisville is not too far.

Nick;
I don't know why the carb diet works. I do know that some cancers depend on their energy from glucose and require a lot of it to reproduce so much more than the rest of the body cells.
The low carb diet works for kids with epilepesy too. Getting rid of the carbs to glucose pathway the body is then forced to produce fat to ketones for energy instead. As a matter of fact the Ketogenic diet up untill the 1930's was the only "cure" and still is for epilepsy. The diet lasted two years and after that there was either a cure of up to 33 percent and improvemnt in up to 70 percent of epileptic patiences.

when I said die off - that was the only description I had -I don't know if it was from something dying off or what in the heck was going off. It is reported a lot by a lot of people and it would sure be interesting if the medical research would find out what is truly going on. I also got at the same time not only every muscle hurting me but a yeast infection which I had not had for a long time, five years since I had started taking vitamin D.

I thought this diet is not working, my husband even said to me, you have killed me. I dug into Dr. Atkins book and he mentions that some of his patience would develop a yeast infection (not the muscle aches) and he said (he really did not know why!) darn!. He did of course have a few thoughts on it ---he thought it was a because the people starting his diet had not eaten cheeses in a long time (that was true in our case) and it was not really a yeast infection but an allergic reacton to what the body thought was a yeast infection from the cheese. True we had ate fetta cheese the night before or maybe it was blue cheese. I don't remember except we were following his two week menu plan trying to learn the basics of the diet, and how to recook.
But it sure felt like and acted like a yeast infection.
As far as pathogen or the vaccine. It took a tetanus vaccine to lay my husband low at at 34. It and it alone I blame. It taxed my husband's system, so he cannot fight off sinus infections, and yet it caused the immune sytem to go overboard in other area and caused it to attack my husband's nerves and muscles. Of course he reacted to a tetanus shot at age 28 that caused him to seize all night long, but he seemed okay after that untill age 34.
So that is why I think it is the vaccine and something in it, but what?

Benedetta,

I wrote:
{I can’t fully explain why the grandchildren and not the children except some inheritances skip a generation}
The other real possible answer is that while this stress changes are also in the parents it is this last generation of kids who have gotten the increased vaccine schedule and that may be what sets off this reaction in those with the most altered gene/dna/chromatin and possibly other particular interacting gene profiles.

Benedetta,

My wife sees a doctor in Louisville, KY who will oversee the Marshall Protocol administration. You have stated you live in KY, but I don't know how close to Louisville you are. If you are close enough, and find you are interested, I can supply contact information. If you are too far away you hopefully could find adductor close to you.

If you read enough at the Marshall site you may have read that he believes the bacteria can affect the genes and cause mutations. This would be one alternate route for such gene changes. I don't rule out their possible involvement and the piece on gene effects and chromatin alteration speak of stresses that can cause this in parents and be passed onto offspring. The piece on Pink Disease and grandparents who had it having grandchildren with much higher Autism rates causes me to think that mercury could have been the progenitor of the stress that could have affected the genes of those grandparents and the grandchildren received these altered genes{ I can’t fully explain why the grandchildren and not the children except some inheritances skip a generation} and were sensitized to environmental stresses and triggers like Alum in vaccines that inordinately altered their immune responses leading to chronic immune reactions including in the brain. But, Mercury could have allowed the bacteria Marshall speaks of to erupt and cause the gene/dna/chromatin stress that gets passed on, or the mercury could have caused the gene/dna/chromatin stress that allows other triggers and toxins in the womb to have negative effects and cause a sensitized child to be born and then the vaccine sends them into hyper deregulation over the long term causing the problems. Yet, it could be vaccines could disrupt the immune system enough to allow the Marshall bacteria to take over and be the main disease causing factor. It could be one then the other or a synergy of both leading to Autism and other disease conditions, but the vaccine reaction accounts from parents point to a major change event right after vaccination. The high levels of Ostopontin in the children with Autism in the study and the fact that higher levels correlated with more severe autism makes me think that at least in large measure the vaccine/Alum {and sometimes other vaccine additives and antigen} is doing something bad all on its own as the IL-17 increase is more likely to come from elevated Osteopontin and the bacteria mainly lowers the TH-1 response. It could be vaccines being the only or worst offender in some cases or the bacteria in others, or both at the same time or in succession with one at work worsening the other and possibly any one of the possible scenarios applying to once child and a different one to another . This might be part of the reason for some of the uncertainty as to what is causing inflammation you may find in my posts.

I don’t think Olmesartan alone can deal with all the problems in many cases of Autism. It may help a great deal in many cases, but I am confident other treatment is needed in the majority of cases to see recovery, because the problems that may arise from immune dysfunction in Autism lead to enough system alterations and changes bringing about a static malfunction and restoring immune function alone will not usually or totally correct everything. In many other conditions that are not as involved it likely can and does largely reverse the conditions or halt them at least. The fact that many have recovered without Olmesartan means the bacteria are surely not the only cause and not therefore the worst problem in biomedical treatable Autism in kids who have improved greatly or recovered without it. Yet, I can’t rule out that it possibly may be that when offending food antigens and carbohydrate reduction is applied this might stifle bacterial nutrition sources reducing their grip and allow the immune system to focus only on the bacteria and overcome them. But, diet is another treatment. So it is probably helpful in most cases of immune related Autism and is probably the driving factor in a number of other conditions. It has been credited a s being the cure for at least of child with Autism.

Thanks Nick, for explaining so patiently to me.
It is interesting how an environmental impact can make what is already present in our genes to -- as you say loosen or not be as tightly packed.

I see Marshall test for vit D, and have diets that limit vit D.
You said something about die off - we experience that a week after we started the Atkin's diet of only 15 to 20 carbs - it was very painful - every muscle in my body and my husband's body hurt, but my son and daughter did fine, but I think my duaghter cheated.
Friut fly genes after a few generation were able to go revert back to normal, but being fruit flies - I am not sure humans are as resilent - for my family it looks like there will be no new generations.
I still have some more reading to do over at Marshalls.
Thanks again.

Benedetta,

I will go ahead with some thoughts on vitamin D, but it might be good to know the age, problems, and a little of your children’s and your medical history including diagnosed Autism and bi-polar. I think you have mentioned those conditions as being in your family, but I don't recall who has what. I am not asking this to offer some diagnosis, but to try to better relate the medical symptoms to vitamin D. You did mention a few and said your family feels better on it.

While I have seen the Marshall Protocol work for my wife, and value Dr. Marshall’s theory and insights, I am not clear on the vitamin D issue in general. I think he confines his theory to vitamin D being bad when one has the bacteria he speaks about and does not imply that vitamin D induces the bacteria generally in otherwise healthy people. Though, it would stand to reason that high doses of vitamin D could lead to immune suppression at the first sign of serious or longer than typical infections.

The information I posted does say; "Synthesis of osteopontin is stimulated by calcitriol (1,25-dihydroxy-vitamin D3)." This is bad if it is true that the high levels Ostopontin in Autism are leading to damaging immune reactions and inflammation as it would be a reason Ostepontin would rise. It is also very interesting to note that the drug used in the Protocol, Olmesartan, is listed in the Ostepontin post information as a reducer of Osteopontin levels. This could explain some of its positive effect in brain function. The Olmesartan effectively clears and binds to the VDR to promote the Th-1 immune response to begin clearing the pathogens. This is a slow process and can take years and produces some difficult “healing “ periods as killing off the pathogens produces products and immune response effects itself, but the cure is better than the disease and you are getting better over time and not worse. It is akin to “die off” that you are probably familiar with and can produce flu-like symptoms and sometimes bad flu like symptoms. The regimen is calls for reaching a level of “die off “symptoms that are not too bad by the dosage level of the Olmesartan. My wife has been on it about 15 months and the first 3 months were pretty rough and then she reached a dosage that w as better. But by 10-11 months she had some pretty bad times. But in the last4-5 months she has done better than ever. She is still slowly seeing improvement

The Marshall theory states that certain types/forms of bacteria "infect certain cells in the body particularly some immune cells and that these bacteria can block the VDR in cells. This inhibits the production of immune responses that will kill these bacteria leading to an increase in the bacterial numbers and eventually a disease process that lead to many different "autoimmune conditions and disease. It also holds that this disrupts all sorts of other systems in the body and leads to numerous symptoms including human steroid and hormone changes and disruption. It proposes that it can contribute or be involved in bi-polar autism and other "mental disease/illnesses". In short, if unchecked they may lead to serious health problems.

I have recently stated that I felt that something must be happening to open the door for them to get started taking over some aspects of immune reaction, but his literature does mention some things that can start or promote their becoming pathogenic, so I have no problem with that after all. I do think that the Alum and other affects of vaccine components can be a major widely encountered immune deregulator that allows them to take hold.

Just because the VDR is blocked this does not mean that one would not have allergies. The idea in the Protocol is that the increasing bacteria and immune inhibition of TH-1 {though other immune factors are involved} allows for affects that can lead to allergies. If such a process is occurring and you take vitamin D the idea is that its function as a secosteriod can reduce the inflammation and lessen the immune response, but this actually facilitates the progression of the bacterial encroachment in immune function. This may be a very slow process, so people who having milder problems may start vitamin D and find their problems calm down greatly, but are setting themselves up for much worse problems when the pathogens reach a certain point of integration in one's system and then people will start reaching for medicinal steroids or be popping anti-inflammatory medications to treat the symptoms. So, by theory vitamin D in such affected people is normally a problem and should not be supplemented.

Yet, the conflicting studies on the benefits of vitamin D leave some questions about what possible exceptions may exist to his theory. By the way I totally agree with the thought that vitamin D may be being used by some other system in the body and I have been looking at this for a while, but no clear answer yet. I cannot make any guarantee anything, but the fact vitamin D “palliates your family’s symptoms and the fact they return when you don’t take it may mean the problems that cause the original problems are there and could be being made worse over time by the vitamin D supplementation. As, I said a over a year ago in our exchange on this thread my wife’s problems were pretty bad and additional D made her worse over time. I think that means her pathogen load was already so high that the D could not mask the issue and was allowing the bacteria to proliferate making her worse. The confounding part of your situation to me is that yeast problems return without vitamin D. The only thing I can think of is that D in your case may increase certain bacteria in your gut that and mucosal tissues that suppress yeast growth, but that is conjecture.

I highly recommend that you go to the Marshall Protocol website and read firsthand what it is about. It would be good to a t least read the sections I mention below and there is a "Knowledge database" that is helpful for questions you may have. There is quite a bit there.

At the website:

For Patients

Why microbes may cause chronic inflammatory diseases

Introduction to the Marshall Pathogenesis

Successive infection and variability in disease

Familial aggregation

Transmission of bacteria and onset of disease

Microbes in the human body

Evidence that chronic disease is caused by pathogens

What is the Marshall Protocol? – The cornerstone of the MP is frequent dosing of olmesartan (brand name Benicar), which stimulates the innate immune response.

Introduction

Length – may take several years depending on how sick a patient is

Cost – insurance often pays for certain basic expenses; drugs can be ordered online at a discount

Palliative vs. curative treatments – many widely used treatments and supplements such as vitamin D compromise the immune response to microbes and are therefore contraindicated

http://mpkb.org/

Benedetta,

You said:

"I am still trying to digest what you are saying and the articles are saying."

I am not sure where to start to explain the Osteopontin information further because I am not sure what is not communicated. The information in the article, “The roles of TLRs, RLRs and NLRs in pathogen recognition”, is more about explaining how parts of the immune system function and is a bit of overload to explain the Alum/NALP3 connection. You may need to Wiki a lot of the terms in the article to understand their functions. That is the only way to get a basic grasp on their relation. The effects in one immune component often bear on another and in chronic dysfunction the problems can increase. Trying to narrow down where the immune system is being inordinately perturbed is important to the overall picture.

One point relevant to our interest is the ways vaccines can cause or promote Autism. This is the tie into to the Alum mentioned in the post and in the article tying it to NALP3. Since alum is a strong stimulator to produce immunity if something is sensitized or unusual in a child’s gene expression or chromatin.

While I am not saying Alum{aluminum adjuvant in vaccines} alone causes all Autism or by itself causes Autism in a perfectly healthy child {I am not saying it doesn't either, but not likely imo}, I am saying it may contribute to it or set it off in those who are sensitized or predisposed. I have tried to explain some possible ways that children are sensitized before vaccines are given in previous posts and invoked one such idea at the end of the Osteopontin post when I talked about DNA and posted the article that talked about the nucleic acid release from damaged or dying DNA and RNA and how stopping the inflammatory response to these acids can treat autoimmunity. One way a child could be "sensitized" is that I am talking about was posted earlier.

Please read it in light of what may happen to a child given a vaccine with Alum {other vaccine substances can be involved in immune resposne results too} that has a described chromatin/gene alteration described in the below article.

Scientists discover how we pass on DNA changes caused by stress
"According to the article abstract and other materials provided by Cell Press:
Gene expression of encoded proteins depends upon how genes are chemically repackaged into more complex chromatin structures. But in some sections of the genome, genes are repackaged extra-tightly into heterochromatin structures that are passed intact to the next generation, usually without any active genes.
The researchers had discovered 20 years ago in studies of the unicellular organism yeast that a gene known as activation transcription factor-2 (ATF-2) must be present for the tightly-wound heterochromatin packages of suppressed genes to form.
But they found environmental stress, inflammation and oxidative stress activated protein kinases (enzymes that modify protein production by adding a phosphate group), altering ATF-2 and disrupting heterochromatin formation in yeast cells.
To test if this mechanism also activates in multicellular organisms, the researchers turned to fruit flies, because, like yeast cells and humans, these rapidly gestating insects (and favorite genetic test-subjects) carry the ATF-2 gene.
From the new tests, they found that the ATF-2 gene changes and heterochromatin disruption also occurred in the fruit fly embryos exposed to experimental stresses, and found that this mechanism released the inactive genes (that would have remained silent within heterochromatin "packages"), modifying the genomic structure of the organisms, introducing changes that were passed to future generations.
However, these changes were transmitted in a non-Mendelian mode, and the defective heterochromatin gradually reverted to normal over multiple generations.
On the basis of this new research, the scientists speculated similar epigenetic changes in humans could result in inherited impairments in cellular function, metabolism and behavior, and corresponding predispositions to "lifestyle diseases," such as diabetes and heart disease and psychological disorders, such as schizophrenia."

Autoimmunity {if that is the true description for this provoked reaction} is clearly {to me}part of the problem in much Autism. This is especially suspect in those who have strong inflammatory reactions to vaccines. If you have any specific question in trying to understand what I am saying feel free to ask.

My posting of Alum in vaccines being able to raise Ostepontin levels that can trigger IL-17 immune responses involved in “autoimmunity” relates directly to you said recently and points to a very plausible way that a vaccine can cause inflammation. This inflammation does not stop in chronic activation and the high Osteopontin levels in the Autism group mentioned in the study may be an indication of this inflammation. It indeed may be tied to other inflammatory diseases stemming from Alum in vaccines.

You said:

"What I believe and know Nick is that vaccine reaction caused an inflammatory response in my kids, husband and mother.
I believe that inflammatory diseases are rampant and not just affecting the kids with autism."

I will address you vitamin D question in the next post except to say the following:

The Marshall protocol is probably the main reason that vitamin D is avoided by some parents in treating their children with immune related Autism and the evidence from studies is not conclusive that vitamin D always bad or always good. In fact reports abound that it is beneficial to increase it for some conditions. But, in the next post I will try to speak to your concerns and thoughts about it.

I was thinking on the vit D that was mentioned. It sound like vit D is involved in making something that is part of the problem ???

But vit D does help my family.

Then I thought it could be an absorption problem,all the vit D is going into making something that it shouldn't make too much of, depleting the vit D, not leaving enough vit D for the other important functions it is needed for.

This seems to happen a lot to the other vitamins too.
Example there is a build of vit B 12 in the blood of kids with autism as Dr. Wakefield found, but they have a kind of anemnia that comes about because of lack of vit B 12.

If I do not have an excess of vit D in my family's system:
Examples of what happesn:
I want a yeast infection in the fall after spending lots of time in the sun during the summer - All I have to do is not take vit D 4000mg.

If I want my daughter to have an allergy reaction with the cat on the back porch - don't give her vit D.

If I want my son or husband to have some sort of infection in their sinuses or ears don't give them vit D.

Of course this is only one asspect of what is going on.

Nick;
GH commented about this very thing under the article:

http://www.ageofautism.com/2011/08/doctors-on-autism-environment-tightrope-dr-perri-klass-in-nyt.html#comments

I am still trying to digest what you are saying and the articles are saying. Sounds interesting.

I posted the first rendition the post very early this morning, but saw some things that needed fixing, so I posted a corrected version later this morning.

Nod 1 & 2 and many other proteins and pathways are involved, but I was trying to reduce it down to the most associable components.
To simplify the most distilled kernel of thought from that post I will list this linkage.

Alum -> NALP3 -> IL-1β{and others}-> Osteopontin -> IL-17 -> autoimmunity{and brain-specific auto-antibodies}.

The adaptive and innate systems are linked. Here is a piece of an earlier linked article in this thread. TH-17/IL-17 is suggested as a bridge between the adaptive and innate immune systems. The Alum - NALP3 - Osteopontin IL-1B - TH-17/IL-17 affect speaks to a disturbance in the immune system bringing on autoimmunity and immune disequilibrium in inflammation and protective immunity affecting both the innate and adaptive immune systems producing 1L-17 and I think explaining much of what I have posted and linked to in this thread.

Precarious Balance: Th17 Cells in Host Defense

"Lineage-specific responses from the effector T-cell repertoire form a critical component of adaptive immunity. The recent identification of Th17 cells—a third, distinct lineage of helper T cells—collapses the long-accepted paradigm in which Th1 and Th2 cells distinctly mediate cellular and humoral immunity, respectively. In this mini review, we discuss the involvement of the Th17 lineage during infection by extracellular bacteria, intracellular bacteria, and fungi. Emerging trends suggest that the Th17 population bridges innate and adaptive immunity to produce a robust antimicrobial inflammatory response. However, because Th17 cells mediate both host defense and pathological inflammation, elucidation of mechanisms that attenuate but do not completely abolish the Th17 response may have powerful implications for therapy."

http://iai.asm.org/cgi/content/full/78/1/32

Whatever is the actual interaction of Chromatin, DNA, and gene expression that may help bring about a heightened susceptibility whether pre or post vaccination with Alum may be, the trail leading back to Alum in vaccines generating immune dysfunction appears to be demonstrable. It is possible the vaccine themselves are having a trans-generational and/or epigenetic inheritance effect causing increasing DNA stress changes due to the earlier mention piece on ATF-2, but most likely there are other elements causing this or additionally contributing as well.

I had come across Osteopontin some time ago, but the new information from two sources gives the tie I had not seen to Th-17/IL-17 that I have been finding much connection with in the scenario I have thought to exist. I think every word of these articles is a must read.

One of the sources was linked at the Marshall Protocol forum and I will list it first.

Increased serum Osteopontin levels in autistic children: Relation to the disease severity.

Abstract
“Autoimmunity to brain may play an etiopathogenic role in autism. Osteopontin is a pro-inflammatory cytokine that has been shown to play an important role in various autoimmune neuroinflammatory diseases. Osteopontin induces IL-17 production by T-helper 17 lymphocytes, the key players in the pathogenesis of autoimmune disorders. Anti-osteopontin treatment reduces the clinical severity of some autoimmune neuroinflammatory diseases by reducing IL-17 production. We are the first to measure serum osteopontin levels, by ELISA, in 42 autistic children in comparison to 42 healthy-matched children. The relationship between serum osteopontin levels and the severity of autism, which was assessed by using the Childhood Autism Rating Scale (CARS), was also studied. Autistic children had significantly higher serum osteopontin levels than healthy controls (P<0.001). Increased serum osteopontin levels were found in 80.95% (34/42) of autistic children. Children with severe autism had significantly higher serum osteopontin levels than patients with mild to moderate autism (P=0.02). Moreover, serum osteopontin levels of autistic patients had significant positive correlations with CARS (P=0.007). In conclusions, serum osteopontin levels were increased in many autistic children and they were significantly correlated to the severity of autism. Further wide-scale studies are warranted to shed light on the etiopathogenic role of osteopontin in autism and to investigate its relation to IL-17 and brain-specific auto-antibodies, which are indicators of autoimmunity, in these patients. The therapeutic role of anti-osteopontin antibodies in amelioration of autistic manifestations should also be studied.”

http://www.ncbi.nlm.nih.gov/pubmed/21521652

Wiki - Osteopontin
Biosynthesis

"Osteopontin is biosynthesized by a variety of tissue types including fibroblasts[19] preosteoblasts, osteoblasts, osteocytes, odontoblasts, some bone marrow cells, hypertrophic chondrocytes, dendritic cells, macrophages,[20] smooth muscle,[21] skeletal muscle myoblasts,[22] endothelial cells, and extraosseous (non-bone) cells in the inner ear, brain, kidney, deciduum, and placenta. Synthesis of osteopontin is stimulated by calcitriol (1,25-dihydroxy-vitamin D3).

Regulation

Regulation of the osteopontin gene is incompletely understood. Different cell types may differ in their regulatory mechanisms of the OPN gene. OPN expression in bone predominantly occurs by osteoblasts and osteocyctes (bone-forming cells) as well as osteoclasts (bone-resorbing cells).[23] Runx2 (aka Cbfa1) and osterix (Osx) transcription factors are required for the expression of OPN [24] Runx2 and Osx bind promoters of osteoblast-specific genes such as Col1α1, Bsp, and Opn and upregulate transcription.[25]

Hypocalcemia and hypophosphatemia (instances that stimulate kidney proximal tubule cells to produce calcitriol (1α,25-dihydroxyvitamin D3)) lead to increases in OPN transcription, translation and secretion.[26] This is due to the presence of a high-specificity vitamin D response element (VDRE) in the OPN gene promoter.[27][28][29]

Extracellular inorganic phosphate (ePi) has also been identified as a modulator of OPN expression.[30]

"Stimulation of OPN expression also occurs upon exposure of cells to pro-inflammatory cytokines,[31] classical mediators of acute inflammation (e.g. tumour necrosis factor α [TNFα], infterleukin-1β [IL-1β]), angiotensin II, transforming growth factor β (TGFβ) and parathyroid hormone (PTH),[32][33] although a detailed mechanistic understanding of these regulatory pathways are not yet known. Hyperglycemia and hypoxia are also known to increase OPN expression.[32][34][35]"

http://en.wikipedia.org/wiki/Osteopontin

The roles of TLRs, RLRs and NLRs in pathogen recognition
“Alum, which is sensed by NALP3, is widely used as an adjuvant in human, and is known to trigger local recruitment of monocytes and migration into the draining lymph node to prime T cells as well as promote migration of myeloid cells to the spleen to activate antigen-specific B cells. Alum can increase the production of IL-1β via the NALP3 inflammasome as well as via phagocytosis. The production of antigen-specific antibodies following immunization of antigen given in alum was abrogated in mice lacking a component of the NALP3 inflammasome, suggesting the importance of the NALP3 inflammasome in shaping adaptive immune responses (109, 202, 203); however, there is another report showing an indispensable role of the NALP3 inflammasome in alum-induced boosting of antibody production (204). These differences may come from the dose of antigen and adjuvant used, the type of antigen, the route of immunization and immunization protocol.”

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2721684/

This was also posted at the Marshall forum. It just points out one way in which Olmesartan may be helping in some Autism as it lowers osteopontin in the trial. It does other things that are very beneficial in inflammatory conditions though.

Angiotensin II receptor blocker and statins lower elevated levels of osteopontin in essential hypertension--results from the EUTOPIA trial.

BACKGROUND:
Osteopontin is a pleiotropic cytokine that has been implicated as a key factor in the development of atherosclerosis, a major complication of hypertension. We have earlier shown that olmesartan reduces mediators of vascular inflammation in patients with hypertension and cardiovascular disease. We aimed at studying the effect of olmesartan and/or pravastatin on osteopontin plasma levels, and the association between vascular inflammation markers and osteopontin in hypertensive patients.
METHODS:
We assessed a panel of vascular inflammation markers and osteopontin during 12 weeks of therapy with 20mg olmesartan (n=94) or placebo (n=96) in a prospective, double-blind, multi-center study in patients with essential hypertension (re-evaluation of the EUTOPIA trial blood samples). Pravastatin (20mg) was added to the double-blind therapy at week 6 in both arms. The association of demographic variables and inflammation markers with osteopontin has been analyzed as well.
RESULTS:
Baseline osteopontin plasma concentrations in the study population were elevated compared to healthy controls (32.85+/-19.04ng/mL vs. 23.82+/-3.69ng/mL, p=0.027). Mono-therapy with olmesartan and co-therapy with pravastatin reduced levels of circulating osteopontin (p<0.001). The addition of pravastatin to the placebo treatment-arm resulted in a reduction of osteopontin levels as well (p<0.01). osteopontin plasma levels correlated with VCAM-1 (r=0.27; p=0.0002), ICAM-1 (r=0.18; p=0.015), IL-6 (r=0.35; p<0.0001) and hsCRP (r=0.22; p=0.0022).
CONCLUSION:
We show, for the first time, that olmesartan significantly decreases osteopontin concentrations. Co-therapy with pravastatin also reduces osteopontin levels. Elevated osteopontin levels in hypertensive patients correlate with adhesion molecules and inflammation markers.

http://www.ncbi.nlm.nih.gov/pubmed/19801149
To put a very important concept into perspective here is what can be considered as model of how Alum and vaccines can end up promoting Autism and other inflammatory conditions by considering an implication that emerges when taking some points that relate to each other from each of the above articles.
1. Autistic children had significantly higher serum osteopontin levels than healthy controls
2. Alum, which is sensed by NALP3, is widely used as an adjuvant in humans…..
3. “suggesting the importance of the NALP3 inflammasome in shaping adaptive immune responses”
4. Alum can increase the production of IL-1β via the NALP3
5. "Stimulation of osteoponin expression also occurs upon exposure of cells to pro-inflammatory cytokines,[31] classical mediators of acute inflammation (e.g. tumour necrosis factor α [TNFα], infterleukin-1β [IL-1β]), angiotensin II
6. Osteopontin induces IL-17 production by T-helper 17 lymphocytes, the key players in the pathogenesis of autoimmune disorders.
7. Moreover, serum osteopontin levels of autistic patients had significant positive correlations with CARS (P=0.007). In conclusions, serum osteopontin levels were increased in many autistic children and they were significantly correlated to the severity of autism. Further wide-scale studies are warranted to shed light on the etiopathogenic role of osteopontin in autism and to investigate its relation to IL-17 and brain-specific auto-antibodies, which are indicators of autoimmunity, in these patients.

Taken on balance this tends towards confirming my belief that the Marshall pathogens get heavily involved in many cases after certain vaccines with Alum and possibly still due to other vaccine effects as the NALP3 may be altered and this alters the adaptive immune system and the ways it deals with antigens in general leading to chronic "autoimmunity". The Alum may be the worst offender in opening the door for the "infestation".

On top of this another earlier cited report in this thread spoke of DNA release due to Alum in a vaccine as what helped it work. Once the Alum does it’s at least two fold hit it leaves behind likely chronic inflammatory conditions in the susceptible, or maybe just some who happen to be immune stimulated at the time due to a current infection.
New anti-inflammatory agents silence overactive immune response

“DURHAM, N.C. – A new way to fight inflammation uses molecules called polymers to mop up the debris of damaged cells before the immune system becomes abnormally active, researchers at Duke University Medical Center report.
The discovery, published Monday in the journal Proceedings of the National Academy of Sciences, offers a promising new approach to treat inflammatory auto-immune disorders such as lupus and multiple sclerosis, which are marked by an overactive immune response.
"Depending on the disease, cells that are damaged drive or perpetuate the immune response," said Bruce A. Sullenger, Ph.D., director of the Duke Translational Research Institute and senior author of the study. "We have shown that we can inhibit that process."
Sullenger said the idea for the new approach stems from earlier findings by Duke scientists and others that dying and diseased cells spill nucleic acids – the building blocks of life that include DNA and RNA – that then circulate at high levels in the bloodstream.
While DNA and RNA inside the cell regulate important functions such as growth and division, outside of cells in the blood, these nucleic acids serve as powerful signals to the immune system that something is amiss. Once activated, the immune system launches an attack to fight whatever caused the cell damage, whether an infection or toxic substance. Under normal circumstances, this inflammatory response eventually restores order.
In some cases, however, the inflammatory response becomes persistent and out of control, leading to tissue damage and causing symptoms such as fever and pain. Chronic inflammation has been implicated in lupus, multiple sclerosis, obesity, psoriasis, irritable bowel syndrome, arthritis and numerous other maladies.
The Duke scientists, working to interrupt this cycle, focused on a set of molecules called nucleic acid binding polymers that were designed to infiltrate the nucleic acid inside of cells and deactivate specific immune triggers.
"Then we had a 'eureka moment,'" Sullenger said. "Because the inflammatory nucleic acids are outside of cells, whereas DNA and RNA normally function inside cells, we realized that the polymers could bind to the external nucleic acids without disrupting intracellular functions of DNA and RNA."
It was a simple mop-up approach, and it worked as planned in experiments on mice: "We could use the polymers as molecular scavengers - sponges to go around and soak up and neutralize those inflammatory nucleic acids so the immune system doesn't recognize them and go into the overdrive of inflammation," Sullenger said.
David S. Pisetsky, M.D., Ph.D., a rheumatologist at Duke and co-author of the study, said the anti-inflammatory approach has numerous potential applications, not only for auto-immune disorders, but also for the acute tissue damage of severe bacterial and viral infections, shock and injuries.
"One setting to test the effects of the polymers involves acute events such as injuries, where it may be easier to measure the presence of the nucleic acids in the blood and the effects of polymer binding," Pisetsky said, adding that the long-term safety of the new anti-inflammatory approach in humans remains unknown.”

http://www.eurekalert.org/pub_releases/2011-08/dumc-naa081211.php

Whatever the interaction of Chromatin, DNA, and gene expression that may help arrive at a heightened susceptibility, whether pre or post vaccination with Alum, the trail leading back to to Alum in vaccines appears to be demonstrable. It is possible the vaccine themselves are having an intergenerational effect causing increasing DNA stress changes due to the earlier mention piece on ATF-2, but most likely there are other elements causing this or additionally contributing as well.

I had come across Osteopontin some time ago, but the new information from two sources gives the tie I had not seen to Th-17/IL-17 that I have been finding much connection with in the scenario I have thought to exist. I think every word of these articles is a must read. Please note the bolded words as they stress some of the Alum connecting elements to the immune events and the many things throughout the thread, especially those dealing with TH-17/IL-17.
One of the sources was linked at the Marshall Protocol forum and I will list it first.

Increased serum Osteopontin levels in autistic children: Relation to the disease severity.

Abstract
“Autoimmunity to brain may play an etiopathogenic role in autism. Osteopontin is a pro-inflammatory cytokine that has been shown to play an important role in various autoimmune neuroinflammatory diseases. Osteopontin induces IL-17 production by T-helper 17 lymphocytes, the key players in the pathogenesis of autoimmune disorders. Anti-osteopontin treatment reduces the clinical severity of some autoimmune neuroinflammatory diseases by reducing IL-17 production. We are the first to measure serum osteopontin levels, by ELISA, in 42 autistic children in comparison to 42 healthy-matched children. The relationship between serum osteopontin levels and the severity of autism, which was assessed by using the Childhood Autism Rating Scale (CARS), was also studied. Autistic children had significantly higher serum osteopontin levels than healthy controls (P<0.001). Increased serum osteopontin levels were found in 80.95% (34/42) of autistic children. Children with severe autism had significantly higher serum osteopontin levels than patients with mild to moderate autism (P=0.02). Moreover, serum osteopontin levels of autistic patients had significant positive correlations with CARS (P=0.007). In conclusions, serum osteopontin levels were increased in many autistic children and they were significantly correlated to the severity of autism. Further wide-scale studies are warranted to shed light on the etiopathogenic role of osteopontin in autism and to investigate its relation to IL-17 and brain-specific auto-antibodies, which are indicators of autoimmunity, in these patients. The therapeutic role of anti-osteopontin antibodies in amelioration of autistic manifestations should also be studied.”

http://www.ncbi.nlm.nih.gov/pubmed/21521652

Wiki - Osteopontin
Biosynthesis

"Osteopontin is biosynthesized by a variety of tissue types including fibroblasts[19] preosteoblasts, osteoblasts, osteocytes, odontoblasts, some bone marrow cells, hypertrophic chondrocytes, dendritic cells, macrophages,[20] smooth muscle,[21] skeletal muscle myoblasts,[22] endothelial cells, and extraosseous (non-bone) cells in the inner ear, brain, kidney, deciduum, and placenta. Synthesis of osteopontin is stimulated by calcitriol (1,25-dihydroxy-vitamin D3).

Regulation

Regulation of the osteopontin gene is incompletely understood. Different cell types may differ in their regulatory mechanisms of the OPN gene. OPN expression in bone predominantly occurs by osteoblasts and osteocyctes (bone-forming cells) as well as osteoclasts (bone-resorbing cells).[23] Runx2 (aka Cbfa1) and osterix (Osx) transcription factors are required for the expression of OPN [24] Runx2 and Osx bind promoters of osteoblast-specific genes such as Col1α1, Bsp, and Opn and upregulate transcription.[25]

Hypocalcemia and hypophosphatemia (instances that stimulate kidney proximal tubule cells to produce calcitriol (1α,25-dihydroxyvitamin D3)) lead to increases in OPN transcription, translation and secretion.[26] This is due to the presence of a high-specificity vitamin D response element (VDRE) in the OPN gene promoter.[27][28][29]

Extracellular inorganic phosphate (ePi) has also been identified as a modulator of OPN expression.[30]

"Stimulation of OPN expression also occurs upon exposure of cells to pro-inflammatory cytokines,[31] classical mediators of acute inflammation (e.g. tumour necrosis factor α [TNFα], infterleukin-1β [IL-1β]), angiotensin II, transforming growth factor β (TGFβ) and parathyroid hormone (PTH),[32][33] although a detailed mechanistic understanding of these regulatory pathways are not yet known. Hyperglycemia and hypoxia are also known to increase OPN expression.[32][34][35]"

http://en.wikipedia.org/wiki/Osteopontin

The roles of TLRs, RLRs and NLRs in pathogen recognition
“Alum, which is sensed by NALP3, is widely used as an adjuvant in human, and is known to trigger local recruitment of monocytes and migration into the draining lymph node to prime T cells as well as promote migration of myeloid cells to the spleen to activate antigen-specific B cells. Alum can increase the production of IL-1β via the NALP3 inflammasome as well as via phagocytosis. The production of antigen-specific antibodies following immunization of antigen given in alum was abrogated in mice lacking a component of the NALP3 inflammasome, suggesting the importance of the NALP3 inflammasome in shaping adaptive immune responses (109, 202, 203); however, there is another report showing an indispensable role of the NALP3 inflammasome in alum-induced boosting of antibody production (204). These differences may come from the dose of antigen and adjuvant used, the type of antigen, the route of immunization and immunization protocol.”

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2721684/

This was also posted at the Marshall forum. It just points out one way in which Olmesartan may be helping in some Autism as it lowers osteopontin in the trial. It does other things that are very beneficial in inflammatory conditions though.

Angiotensin II receptor blocker and statins lower elevated levels of osteopontin in essential hypertension--results from the EUTOPIA trial.

BACKGROUND:
Osteopontin is a pleiotropic cytokine that has been implicated as a key factor in the development of atherosclerosis, a major complication of hypertension. We have earlier shown that olmesartan reduces mediators of vascular inflammation in patients with hypertension and cardiovascular disease. We aimed at studying the effect of olmesartan and/or pravastatin on osteopontin plasma levels, and the association between vascular inflammation markers and osteopontin in hypertensive patients.
METHODS:
We assessed a panel of vascular inflammation markers and osteopontin during 12 weeks of therapy with 20mg olmesartan (n=94) or placebo (n=96) in a prospective, double-blind, multi-center study in patients with essential hypertension (re-evaluation of the EUTOPIA trial blood samples). Pravastatin (20mg) was added to the double-blind therapy at week 6 in both arms. The association of demographic variables and inflammation markers with osteopontin has been analyzed as well.
RESULTS:
Baseline osteopontin plasma concentrations in the study population were elevated compared to healthy controls (32.85+/-19.04ng/mL vs. 23.82+/-3.69ng/mL, p=0.027). Mono-therapy with olmesartan and co-therapy with pravastatin reduced levels of circulating osteopontin (p<0.001). The addition of pravastatin to the placebo treatment-arm resulted in a reduction of osteopontin levels as well (p<0.01). osteopontin plasma levels correlated with VCAM-1 (r=0.27; p=0.0002), ICAM-1 (r=0.18; p=0.015), IL-6 (r=0.35; p<0.0001) and hsCRP (r=0.22; p=0.0022).
CONCLUSION:
We show, for the first time, that olmesartan significantly decreases osteopontin concentrations. Co-therapy with pravastatin also reduces osteopontin levels. Elevated osteopontin levels in hypertensive patients correlate with adhesion molecules and inflammation markers.

http://www.ncbi.nlm.nih.gov/pubmed/19801149
To put a very important concept into perspective here is what can be put considered from a few point of the above articles tied together”

1. Autistic children had significantly higher serum osteopontin levels than healthy controls

2. Alum, which is sensed by NALP3, is widely used as an adjuvant in humans…..

3. “suggesting the importance of the NALP3 inflammasome in shaping adaptive immune responses”

4. Alum can increase the production of IL-1β via the NALP3
5. "Stimulation of osteoponin expression also occurs upon exposure of cells to pro-inflammatory cytokines,[31] classical mediators of acute inflammation (e.g. tumour necrosis factor α [TNFα], infterleukin-1β [IL-1β]), angiotensin II

5. Osteopontin induces IL-17 production by T-helper 17 lymphocytes, the key players in the pathogenesis of autoimmune disorders.

6. "Moreover, serum osteopontin levels of autistic patients had significant positive correlations with CARS (P=0.007). In conclusions, serum osteopontin levels were increased in many autistic children and they were significantly correlated to the severity of autism. Further wide-scale studies are warranted to shed light on the etiopathogenic role of osteopontin in autism and to investigate its relation to IL-17 and brain-specific auto-antibodies, which are indicators of autoimmunity, in these patients."

Taken on balance this tends towards confirming my beleif that the Marshall pathogens get heavily involved in many cases after certain vaccines with Alum and posibly still due to other vaccine effects as the NALP3 may be altered an this alters the adaptive immune system and the ways it deals with antigens in general leading to chroinc "autoimmunity". The Alum may be the worst offender in opening the door for the "infestation".

On top of this another earlier cited report in this thread spoke of DNA release due to Alum in a vaccine as what helped it work. Once the Alum does it’s at least two fold hit it leaves behind likely chronic inflammatory conditions in the susceptible, or maybe just some who happen to be immune stimulated at the time due to a current infection.

New anti-inflammatory agents silence overactive immune response

“DURHAM, N.C. – A new way to fight inflammation uses molecules called polymers to mop up the debris of damaged cells before the immune system becomes abnormally active, researchers at Duke University Medical Center report.
The discovery, published Monday in the journal Proceedings of the National Academy of Sciences, offers a promising new approach to treat inflammatory auto-immune disorders such as lupus and multiple sclerosis, which are marked by an overactive immune response.
"Depending on the disease, cells that are damaged drive or perpetuate the immune response," said Bruce A. Sullenger, Ph.D., director of the Duke Translational Research Institute and senior author of the study. "We have shown that we can inhibit that process."
Sullenger said the idea for the new approach stems from earlier findings by Duke scientists and others that dying and diseased cells spill nucleic acids – the building blocks of life that include DNA and RNA – that then circulate at high levels in the bloodstream.
While DNA and RNA inside the cell regulate important functions such as growth and division, outside of cells in the blood, these nucleic acids serve as powerful signals to the immune system that something is amiss. Once activated, the immune system launches an attack to fight whatever caused the cell damage, whether an infection or toxic substance. Under normal circumstances, this inflammatory response eventually restores order.
In some cases, however, the inflammatory response becomes persistent and out of control, leading to tissue damage and causing symptoms such as fever and pain. Chronic inflammation has been implicated in lupus, multiple sclerosis, obesity, psoriasis, irritable bowel syndrome, arthritis and numerous other maladies.
The Duke scientists, working to interrupt this cycle, focused on a set of molecules called nucleic acid binding polymers that were designed to infiltrate the nucleic acid inside of cells and deactivate specific immune triggers.
"Then we had a 'eureka moment,'" Sullenger said. "Because the inflammatory nucleic acids are outside of cells, whereas DNA and RNA normally function inside cells, we realized that the polymers could bind to the external nucleic acids without disrupting intracellular functions of DNA and RNA."
It was a simple mop-up approach, and it worked as planned in experiments on mice: "We could use the polymers as molecular scavengers - sponges to go around and soak up and neutralize those inflammatory nucleic acids so the immune system doesn't recognize them and go into the overdrive of inflammation," Sullenger said.
David S. Pisetsky, M.D., Ph.D., a rheumatologist at Duke and co-author of the study, said the anti-inflammatory approach has numerous potential applications, not only for auto-immune disorders, but also for the acute tissue damage of severe bacterial and viral infections, shock and injuries.
"One setting to test the effects of the polymers involves acute events such as injuries, where it may be easier to measure the presence of the nucleic acids in the blood and the effects of polymer binding," Pisetsky said, adding that the long-term safety of the new anti-inflammatory approach in humans remains unknown.”

http://www.eurekalert.org/pub_releases/2011-08/dumc-naa081211.php


I had some déjà vu when reading the following piece and it may be from an ealier expressed sentiment from the same source, but kudos to Johns Hopkins University and David G. Nichols for calling for this overdue new direction. It sounds like the concept I just expressed in a recent post. It is exactly what many of us have been working from for many years and I think they are far more capable at getting at the details with their personnel and resources than we itinerants. If this happens it will be a tremendous achievement that portends a great deal of understanding and treatment for what mainstream medicine has until now missed, misunderstood, and called "idiopathic". I believe they will run head on into what we, or at least some of us, have been saying, about much Autism and by connection "autoimmunity".

Part of the article:

"ScienceDaily (Aug. 18, 2011) — Leaders in biomedical education at Johns Hopkins University School of Medicine are calling for a radical new approach to post-graduate training in the life sciences to address significant challenges, including an avalanche of new discoveries in the last decade and the need to transcend traditional departmental boundaries to understand biological processes at multiple levels.

In a Leading Edge commentary published in the August 19, 2011 edition of Cell, the authors present a new model for biomedical education that would break down current silos of particular disciplines, such as biochemistry, cell biology and physiology, and instead teach students to work across those disciplines to study organisms at all levels, from molecules and cells to an entire organism.

"Increasingly, scientists need a multi-disciplinary approach to answer important questions. They must have the ability to use and interpret information from a wide variety of fields. The current framework for advanced biomedical education, which hasn't changed much in three decades, is no longer suited to helping students integrate the vast amount of knowledge on fundamental biological processes," says David G. Nichols, M.D., M.B.A., vice dean for education at Johns Hopkins who co-authored the commentary.

Currently, most biomedical graduate programs teach first year students in separate silos, giving them separate courses in biochemistry, cell biology, physiology, and so on. The proposed new model would instead divide biology up into the key underlying processes -- gene expression, metabolism and cell fate and function. Instructors would teach each of these key processes, or "nodes," in an integrated bottom-to-top manner, incorporating important information from the molecular scale all the way up to the whole organism."


http://www.sciencedaily.com/releases/2011/08/110818132133.htm

It seemed a natural thought to me when I put up the last post, but in case you don't make the association I am adding this thought.

Some vaccines list glycerin as an ingredient, but I am not sure if any DPT shots have it. But some vaccines list simply gelatin which may be a glycerinated gelatin. This could be a route for glycerol {glycerin, glycerine} to reach the intestines. Also glycerin suppositories, which are often, glycerinated gelatin, are used in infants for constipation and could introduce the substance. If they had a lot of this bacteria it might help cause constipation and a vaccine or suppository containing this could give the bacteria means to produce 1,3-propanediol.

What Is Glycerin (or Glycerine or Glycerol)?

http://www.green-planet-solar-energy.com/what-is-glycerin.html

Benedetta,

I took a quick look and for what it's worth here are a few thoughts on colic and bacteria I belive you are referring to.

I think you are referring to Klebsiella. My son had a lot of colic and I suppose this could be tied to such a bacteria. Different people tend to have different colonization profiles and knowing when this has been "disrupted" from what might have been normal gut colonization for an individual an individual without an atypical alteration or exposure is a hard question to answer without clear markers or testing. The possible interactions with the immune system from the gut and possible bacteria is likely vast, and while colic is not a immediate threat it could signal the beginning of other issues. Is this another variation of an environmentally mediated effect? It could be.

Since you mention the DPT shot I have linked an article relevant to the other things I point to below.

It may be that a concentration of this bacteria in the gut modulates Sphingosine 1-phosphate via the baterial production of 1,3-propanediol. Or through effects on small intestinal lamina propria, but I am not going to comment or add links about the si-lp except to say it relates to retinoic acid and could be worth your while to look into if your son has any current issues.

Here is some info.

Colic In Babies May Be Caused By Gut Bacteria

“During our study, we also found that the babies that didn’t have colic had more types of bacteria in their intestines. The presence of more bacteria may indicate that specific bacterial species (phylotypes) are beneficial to humans,”

http://www.sciencedaily.com/releases/2009/07/090724144520.htm

Klebsiella oxytoca as a Causative Organism of Antibiotic-Associated Hemorrhagic Colitis

http://www.nejm.org/doi/full/10.1056/NEJMoa054765

Glycerol fermentation to 1,3-propanediol by Klebsiella oxytoca NRRL B-199:

http://74.6.238.254/search/srpcache?ei=UTF-8&p=Klebsiella+clostridia&fr=sfp&u=http://cc.bingj.com/cache.aspx?q=Klebsiella+clostridia&d=4868852495679573&mkt=en-US&setlang=en-US&w=fd905a30,abecf77&icp=1&.intl=us&sig=8.F3bOJg1QQ7t3hAexThig--">http://cc.bingj.com/cache.aspx?q=Klebsiella+clostridia&d=4868852495679573&mkt=en-US&setlang=en-US&w=fd905a30,abecf77&icp=1&.intl=us&sig=8.F3bOJg1QQ7t3hAexThig--">http://74.6.238.254/search/srpcache?ei=UTF-8&p=Klebsiella+clostridia&fr=sfp&u=http://cc.bingj.com/cache.aspx?q=Klebsiella+clostridia&d=4868852495679573&mkt=en-US&setlang=en-US&w=fd905a30,abecf77&icp=1&.intl=us&sig=8.F3bOJg1QQ7t3hAexThig--

Sphingosine-1-phosphate receptor agonist and antagonist compounds description/claims

"Sphingosine-1-phosphate (S1P) is part of the sphingomyelin biosynthetic pathway and is known to affect multiple biological processes. S1P is formed through phosphorylation of sphingosine by sphingosine kinases (SK1 and SK2) and it is degraded through cleavage by sphingosine lyase to form palmitaldehyde and phosphoethanolamine or through dephosphorylation by phospholipid phosphatases. It is present at high levels (˜500 nM) in serum, and it is found in most tissues. It can be synthesized in a wide variety of cells in response to several stimuli, which include cytokines, growth factors and G protein-coupled receptor (GPCR) ligands. The GPCRs that bind S1P (currently known as the S1P receptors S1P1-5), couple through pertusis toxin sensitive (Gi) pathways as well as pertusis toxin insensitive pathways to stimulate a variety of processes."

http://www.freshpatents.com/-dt20090129ptan20090029947.php

Cutting Edge: Alternative Signaling of Th17 Cell Development by Sphingosine 1-Phosphate1

http://www.jimmunol.org/content/178/9/5425.full

Sphingosine 1-phosphate dependence in the regulation of lymphocyte trafficking to the gut epithelium

In addition, a recent study demonstrated that oral administration of deoxypyridoxine (DOP), which is a vitamin B6 antagonist, increases S1P concentration in the thymus and secondary lymphoid organs by inhibiting S1P degradation (23). This increased S1P concentration causes lymphocytes to accumulate in the thymus and simultaneously to be depleted from the blood and lymph (23). We recently revealed that S1P also plays an important role in the regulation of peritoneal B cell trafficking into intestinal compartments for intestinal secretory IgA production (24). Although these findings suggest that S1P plays an essential role in the regulation of lymphocyte trafficking in both systemic and mucosal immunity, its involvement in IEL trafficking remains largely unknown.

http://jem.rupress.org/content/204/10/2335.full

Just linking this for a possible link to the heart and the other things discussed.

Sphingosine-1-phosphate receptor signaling in the heart

"The five known members of the sphingosine-1-phosphate (S1P) receptor family exhibit diverse tissue expression profiles and couple to distinct G-protein-mediated signalling pathways. S1P1, S1P2, and S1P3 receptors are all present in the heart, but the ratio of these subtypes differs for various cardiac cells. The goal of this review is to summarize data concerning which S1P receptor subtypes regulate cardiac physiology and pathophysiology, which G-proteins and signalling pathways they couple to, and in which cell types they are expressed. The available information is based on studies using a lamentably limited set of pharmacological agonists/antagonists, but is complemented by work with S1P receptor subtype-specific knockout mice and sphingosine kinase knockout mice. In cardiac myocytes, the S1P1 receptor subtype is the predominant subtype expressed, and the activation of this receptor inhibits cAMP formation and antagonizes adrenergic receptor-mediated contractility. The S1P3 receptor, while expressed at lower levels, mediates the bradycardic effect of S1P agonists. Studies using knockout mice indicate that S1P2 and S1P3 receptors play a major role in mediating cardioprotection from ischaemia/reperfusion injury in vivo. S1P receptors are also involved in remodelling, proliferation, and differentiation of cardiac fibroblasts, a cell type in which the S1P3 receptor predominates. Receptors for S1P are also present in endothelial and smooth muscle cells where they mediate peripheral vascular tone and endothelial responses, but the role of this regulatory system in the cardiac vasculature is unknown. Further understanding of the contributions of each cell and receptor subtype to cardiac function and pathophysiology should expedite consideration of the endogenous S1P signalling pathway as a therapeutic target for cardiovascular disease."

http://cardiovascres.oxfordjournals.org/content/82/2/193.full

Nick:
You talk of gut.

A recent study came out about the cause of colic in babies - maybe over six months ago. The cause they said was a wrong kind of bacteris in the gut. I forgot the name of the bacteria. I did not try to find the report, just heard it on the news briefly.

My duaghter did not have colic, she was not doing well with her DPT shots, but at least it was not obvious to me at the time and she did better with them than my son who did have colic and reacted to his very first DPT shot with heart problems.

Daniel Tammet England's brainman- He is an autistic servant, I saw him on a TV shot he can - learn a foreign language in one week and they showed him learning the language of Iceland and then was put on an Islandic news station to converse with them in their language all in just a week later! His mother said he had colic really bad as a baby (of course they would not mention a vaccine was involved so we only get partial information) but she said he one day had a seizure and as a baby became autistic, and then he outgrew it. He was left with perfect recall of math and learning of languages.

Colic- there is no doubt that the babies stomachs hurt. THey draw their legs up on their belly, they cry almost nonstop, they will sleep only in an inclined position, and some women (not me) have a nack of getting that belly in the right position on their hip and getting them to stop crying.

Maybe there are some answers there?

Benedetta,

You wrote:

“What in the vaccines did the teaching? Hg or Al or sequalene or proteins from dead viruses, or proteins from sneaky live viruses that is not suppose to be there, or proteins hung onto Al salts, or proteins hung on to Al salts with some mercury thrown into the mix?”
That is a fairly new thought about a possible harmful component, and while I think viruses are involved in some cases in the womb or even where you point to possibly in vaccines here again we need to try to understand how these pathogens could affect the system. The maze is filled with openings in Autism causation or synergistic possibilities. Since viruses are implicated in some cancers they demonstrate their ability to have a powerful effect. All sorts of toxins can have these effects as well. I will throw out this little bit that lightly addresses an area in which viruses and toxins {including metals like Al and HG} can have an effect. Dr. Marshall’s proposal offers a rational for such effects as well and they focus on a type of bacterial involvement.

Again from a couple of posts back I wrote: "or types of increasing or previously absent environmental stressors may interact with the effected protein kinase{s} in offspring."

For example:

Effects of heavy metals on mitogen-activated protein kinase pathways

"Consequently, various cellular responses may be caused by the distinct pattern of MAPKs activation. MAPKs may be one of the important cellular signal transduction pathways affected by various environmental pollutants, including heavy metals."

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2723471/

It is also plausible that the pathogenic affect of the bacteria Marshall explains may cause this affect or have the door opened to them drastically elevating this process. If the process starts with mercury, and or say aluminum via disruptions in innate immunity related to possible gene issues, or other exposure this could be how the pathogens gain access to be a chronic problem in many cases and become a part, or the greater part, of the problem for a portion. From how I read his work he thinks they cause the problem from the beginning. I have thought that something else opens the door for them whether it is changes in our environment that promotes this bacterial "infestation", elements that change the body chemistry like SSRI’s and other drugs alter metabolism and neurotransmitter functions that promotes the process, changes to gut ecology by some medicines, immune function affects from vaccines, or a combination, but do believe that often they are a major problem that does great harm and may lead, or help lead, to the conditions of full blown disease states.

You keep at it to Benedetta, the end could be in sight.

Benedetta,

I have no issues with the testimony that people react with damaging inflammatory reactions to some vaccines and that this is often a cumulative in some children. Yet, starting with damaging inflammation and getting to Autism requires a great deal of explanation. You and I are on the same page. I must say though I have to work from circumstantial evidence and testimony from others like you and the Polling’s regarding my wife and the belief vaccines affected her as I did not meet her until she was 16 and had most of the vaccines she has received. But, I find much to support the circumstantial evidence when you look hard at the available information on disease processes and immunity and the accumulated evidence in many studies on “autoimmunity” even if some part of the explanation for autoimmunity is amiss if there is a vaccine connection. Even if I ruled out vaccines it would not change her past, and to some degree, present condition. But, displaying how vaccines that have reportedly played a part, or been the largest or necessary trigger for many with Autism have at least one important purpose. I will try to touch on one purpose at the end of this post.

Please keep in mind when I say "if" regarding something I am discussing in my postings it does mean that I have no opinion or belief about the matter unless I directly say so in regard to the particular thing discussed, nor does it mean I lack a firm conviction as in "I know", but I realize any reading it are only served by reasoning it through on their own as they cannot know simply because I may believe I know. Also, some of what I think I know for some with immune related Autism and immune related problems may not, and almost certainly do not, apply to everyone with Autism.

A couple of things that need to be kept in mind I think are the questions that leap out when easier to observe factors are considered. Most in our community would agree that Autism rates have truly increased and most seem to think they still are increasing. If vaccine rates have been static in the USA for the last 15 years, and looking only at the USA, and Autism rates are still rising we have a couple of major questions to consider. First, why do only certain kids react to vaccines in a way that brings about bad long term consequences and Autism? Second, why are Autism rates, as they appear to be, rising under the same vaccine schedule? If the two ideas in those questions are true, and we rule out a genetic epidemic as the cause, then the most likely reasons that answer those questions are as follows. Something is affecting the systems of those children before vaccination that makes them susceptible to this harm, and whatever is causing this affect is affecting larger numbers of children over time. It may be easiest to think of it as the threshold for damage is being lowered in the population at large or in certain phenotypes being exposed to increasing amounts of what affects their systems in this manner, so that those more inclined to be sensitized due to changes in their biology are increasing vaccine sensitive numbers. In some the changes may become pronounced enough, and their exposures to other environmental stressors may be high enough, that they can have Autism begin to manifest without a vaccine.

As for the importance of the purpose in displaying {explaining how it happens} the vaccine connection instead of simply claiming it I offer this. Science will always pronounce claims as unproven and only pronounce something as repeatable. The inertia against entertaining a relationship of vaccines to Autism exists by the claims that there is no association without repeatable evidence. This is embedded in the media consciousness and is buttressed by many credentialed people and by the form of science they produce. Many of us think/know that their science is lacking, but the only way to cut through this barrier of established thought is through the proposals of causation based on generally proven workings of biology and disease processes along with the accepted concepts of how these systems are disrupted. If we can’t make a case that is compatible with what is known about biology we don’t have much to talk about even “if” our stories are true because they cannot be challenged in most any other way. By documenting the action, effects, and even documented damage that is known or possible by certain elements like vaccines and toxins we can present a reasonableness as to why open minded scientist should look again at our appeal. To give them reason to test our claims in light of other factors that present vaccine damage as plausible and to look at things unknown until recently about vaccine effects to those who have not observed vaccine reactions. The wider public is also important to address and I think they would want a lot of this type of explanation as well. A good scientist would not need to observe every reaction to understand an effect, but I believe the best observers arrive at the best science. This also means anyone reading of our approaches to these matters deserves our most thoughtful and detailed proposals of why the effect happened.

Plus, children's and families well being is at stake.

I hope you understand I do not exonerate vaccines in many cases for “setting off” Autism in my posts nor do I accept that typical gene function and normal generational genetic variations and inheritance is the reason for the rapid rise in Autism. I do find it reasonable that environmental effects prior to vaccines may act more strongly on some to affect their genetics. This same scenario could be applied to many other immune/inflammatory conditions you allude to depending on the effect the environmental stresses have on their phenotype. In many cases a vaccine may be the match. Since I read your question about genes and vaccines in another thread this post can also serve as my answer to what is meant by “genes load the gun and vaccines pull the trigger”.

What I believe and know Nick is that vaccine reaction caused an inflammatory response in my kids, husband and mother.
I believe that inflammatory dieseases are rampant and not just affecting the kids with autism.

There may be and probably are more things that cause inflammatory reactions, than we can possible shake a stick at, but vaccines will be the major cause.

Not a belief but a fact stated in medical text books and college immunology text books that says the immune system is inherited, even the father can and will pass on the way his immune system reacted to certian things.

Vaccines may have taught our immune systems to react a certian way, and perhaps not the best way. What in the vaccines did the teaching? Hg or Al or sequalene or proteins from dead viruses, or proteins from sneaky live viruses that is not suppose to be there, or proteins hung onto Al salts, or proteins hung on to Al salts with some mercury thrown into the mix?

Keep going Nick, let us know what you keep digging up.

I said a few posts back:
"If the mercury connection they cite is true than some effect is reasonable to believe is being passed on, and they do."
This is not saying what I was trying to say.
What I mean is if the effect of mercury in grandparents is related to higher autism rates in grandchildren there would probably have to be way for that to come through the genes, instead of simply mercury being the direct toxin to the fetus passed on in gestation though mothers, and may do so without a classified gene mutation. It may still be called a defect though albeit temporary as it would cease to express after some generations as indicated in the ATF-2 article. If it is passed on though the genes and not a mutation per se, then there must be a possible mechanism explained to achieve the transmission in a non-mendelian manner. If ATF-2 were affected in these grandparents it could be the way this susceptibility is passed on. That is why I linked the article "Scientists discover how we pass on DNA changes caused by stress". It explains how this might occur. The folks who produced the mercury study did not suggest any mechanism as to how the mercury exposure could affect descendants which would likely be what a reader thought I was meaning when I said, “and they do”. These ATF-2 changes might cause genes to be expressed in a future generation that precipitates the silencing of other genes or types of increasing or previously absent environmental stressors may interact with the effected protein kinase{s} in offspring. Though not posited it is appealing to entertain that the mercury and other exposure is responsible for many of the proposed gene dysfuntion explanations and "findings" that are being assoicated with Autism and other immune related conditions that many papers are coming out with currently.

Benedetta,

Since you mention you liked one theory best I would like to say one more thing. I would add, in one sense everything I post I consider as part of one theory that explains the association of dysfunction of many factors and functions of a person’s biology and problems related to autism. If you read the articles and ideas I post you may be able to see how the things I point out or are allude to in the articles are theoretically connected and elaborated upon. Yet, it is possible some of the components I point out might be thought of as standalone theories that one may consider relevant while not seeing others being relevant and this could be the case. Of course many would say none of it is relevant, but that is the ongoing division we deal with on in Autism and biomed. Since the systems of biology all interact at some point trying to understand the relationships, systems, and studies that give light on how these may be affected and cause other dysfunction is quite a maze. This includes gluten, genes, germs, and a host of other things. Keeping all the supportive and confounding information in mind is the challenge. Plus, since there may be numerous triggers or variant problems it increases the difficulty in seeing a sequential pattern and unified theory as to the etiology of Autism. There may be more than a couple of routes to Autism besides the rare gene only caused cases, but even then there may be just one or two offenders or types of insults that lead to Autism through different effects from one individual to the next.

Thanks for the thoughts.

Keep at it Nick;
I do drop by, and read occasionally.
Reading and then summarizing, or writing about our experiences; reading others' thoughts and experiences has and is for me - been healing in some ways, and getting it straighter in my mind.

And sometimes just more confusing too, but that is part of the process, I guess.

Hi Benedetta,

I feel like Tom Hanks in "Castaway"' Up till now I have been talking to "Wilson". So, nice of you to drop by.

The alum does tie into all the immune conncetions and extends to other pathways, but the mercury ties are still relevant I think. It can be both of course. There seem to be multiple offenders, but there are likley just a couple of major ones that set the table. Other offenders may may increase the problem or become problems as a result of the primary problems. A chain reaction it seems.

I don't explain many of the connections I belive are there from the articles I cite, but try to mention enough for the basic connections to be made by those who read the usually brief comments I make. At times I supect some things may only apply to my wife or a very few with Autism, but I cannot know. One such thing is the part about the TB medications her mother had. Even so, it could very well fit into the picture for many thorugh different drugs and substances with similar properties.

It may be something few will do, but reading all the articles or papers linked is needed to get a grasp of why I cite them. I have not had the mental energy to elaborate those connections much and that may make my postings less interesting or may even fail to convey the reason I cite them for many.

I don't know how long I will use this thread as a cork board of thoughts, but it is good to have you drop a line.

So far I like the alum theory best.
Any metal should not be in the body, and vaccines makers have not minded a bit to cross that line with both aluminium salts and mercury.
Years ago on 60 minutes they showed an old couple: the man had Alzheimer's - it was common knowledge back then that they were finding alum in the brains of alzheimer patients. The lady was doing her best to reduce all sources of alum in her cooking - no baking powder, no cooking in alum pots and pans, - she could not understand where this alum was coming from .

I wonder if the vaccine manufactures watching this program and knowing alum was in the vaccines (flu vaccines) were laughing at her ignorance or just simply shugging thier shoulders as "that's is life, nothing personal, just bussiness".

The study link about mercury connection a couple of posts back speaks of grandchildren of those who had pink disease from mercuy sensitivity having much higher rates of autism. It might be good to consider that the mercury effects in previous generations may have a way to be expressed in the genes of descendants without there being a mutation. If the mercury conncetion they cite is true than some effect is reasonable to believe is being passed on, and they do.

Scientists discover how we pass on DNA changes caused by stress
"According to the article abstract and other materials provided by Cell Press:
Gene expression of encoded proteins depends upon how genes are chemically repackaged into more complex chromatin structures. But in some sections of the genome, genes are repackaged extra-tightly into heterochromatin structures that are passed intact to the next generation, usually without any active genes.
The researchers had discovered 20 years ago in studies of the unicellular organism yeast that a gene known as activation transcription factor-2 (ATF-2) must be present for the tightly-wound heterochromatin packages of suppressed genes to form.
But they found environmental stress, inflammation and oxidative stress activated protein kinases (enzymes that modify protein production by adding a phosphate group), altering ATF-2 and disrupting heterochromatin formation in yeast cells.
To test if this mechanism also activates in multicellular organisms, the researchers turned to fruit flies, because, like yeast cells and humans, these rapidly gestating insects (and favorite genetic test-subjects) carry the ATF-2 gene.
From the new tests, they found that the ATF-2 gene changes and heterochromatin disruption also occurred in the fruit fly embryos exposed to experimental stresses, and found that this mechanism released the inactive genes (that would have remained silent within heterochromatin "packages"), modifying the genomic structure of the organisms, introducing changes that were passed to future generations.
However, these changes were transmitted in a non-Mendelian mode, and the defective heterochromatin gradually reverted to normal over multiple generations.
On the basis of this new research, the scientists speculated similar epigenetic changes in humans could result in inherited impairments in cellular function, metabolism and behavior, and corresponding predispositions to "lifestyle diseases," such as diabetes and heart disease and psychological disorders, such as schizophrenia."

http://www.digitaljournal.com/article/308438

The last post contains a basic theory that certainly is basically a thought experiment. I felt I should not have posted it afterwards. But, with the connection I find compelling wiith TH17 and by relation TH1, I find this new relaease today makes the theory a little more plausible as it mentions a linkage beween TH17, PI-3K, and Akt . PTEN is often linked to prostate cancer. That at least has a slight tie to the idea that autism is much higher in boys.
Also, about PTEN Wiki says:

Cell Regeneration
"PTEN's strong link to cell growth inhibition is being studied as a possible therapeutic target in tissues that do not traditionally regenerate in mature animals, such as central neurons. PTEN deletion mutants have recently[8] been shown to allow nerve regeneration in mice.[9]"


A Novel Mechanism That Regulates Pro Inflammatory Cells Is Identified

"Cytokines such as IL-2 or IL-7, which share a common receptor component (called gamma-c) are released by other T cells or specialized non-lymphoid cells. This family of cytokines is critical in the development, survival, proliferation and differentiation of T cell subsets. Gamma-c cytokines activate several signaling pathways within the cells that lead to activation of transcription factors, which then turn on and off specific genes. The researchers found that gamma-c cytokines induced Th17 cell function by activating a specific pathway involving the kinases PI-3K and Akt. They further showed that two transcription factors called FOXO1 and KLF2, which are normally inhibited by PI-3K and Akt activity, suppress the production of Th17 cytokines when overexpressed, even if PI-3K and Akt are fully active. These lines of evidence highlight a novel anti-inflammatory mechanism of action for PI-3K and Akt inhibitors, some of which are in clinical development for cancer-related indications."

http://www.newswise.com/articles/a-novel-mechanism-that-regulates-pro-inflammatory-cells-is-identified

The Pten gene has been associated with some Autism and with some cancer. Here is a theory. It might be that there is a widespread effect on regions of brain cortical cells that is the earliest part of the cancer process. This might be thought of as a very limited diffuse cortical cancer process. The gene expression is primed to these processes with attendant cancer type reactions of inflamation and immune response. Inflamation and immune irregularities are cited by some research on brains of those with autism. This could be tied to dna release, aging,and apoptosis timing alteration. That could be relevant to why brain cells of those with autism grow more quickly and then, from what I have read, parts of the brain shrink more quickly with age.

PTen Gene - Wiki
http://en.wikipedia.org/wiki/PTEN_(gene)

PTEN and the PI3-Kinase Pathway in Cancer

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2710138/

Phosphatidylinositol-3-kinase/Akt/glycogensynthase kinase-3 b and ERK1/2 pathways mediate protective effects of acylated andunacylated ghrelinagainst oxygen-glucose deprivation-inducedapoptosis in primary rat cortical neuronal cells

http://74.6.117.48/search/srpcache?ei=UTF-8&p=Ag-induced+protection&fr=sfp&u=http://cc.bingj.com/cache.aspx?q=Ag-induced+protection&d=4688575520903177&mkt=en-US&setlang=en-US&w=6ee296ce,14fb003d&icp=1&.intl=us&sig=VWRxF5UjTQ.3MoaS8uEjbA--">http://cc.bingj.com/cache.aspx?q=Ag-induced+protection&d=4688575520903177&mkt=en-US&setlang=en-US&w=6ee296ce,14fb003d&icp=1&.intl=us&sig=VWRxF5UjTQ.3MoaS8uEjbA--">http://74.6.117.48/search/srpcache?ei=UTF-8&p=Ag-induced+protection&fr=sfp&u=http://cc.bingj.com/cache.aspx?q=Ag-induced+protection&d=4688575520903177&mkt=en-US&setlang=en-US&w=6ee296ce,14fb003d&icp=1&.intl=us&sig=VWRxF5UjTQ.3MoaS8uEjbA--

Also in the news....Mercury and Autism.

http://www.swinburne.edu.au/chancellery/mediacentre/media-centre/news/2011/08/australian-research-finds-autism-risk-

The assurance that vaccines cannot cause negative long term effects rests upon the notion that they know and have known about the workings of the immune system and it's components so they know what happens when one is vaccinated. Th17 {T helper cells} were only discovered a few years ago and they appear to be quite important in the immune system and vaccine response. IL-17{cytokines} was found in 1993 which is long after vaccines were in use. I have read one casusal admission that they don't know what adjuvants may do in effecting the Th17 lineage and another mentioning a new found effect of the alum adjuvant on DNA. The article doesn't seem to see any possible problem in the DNA effect, but it got my attention.

The article on TH17 and adjuvants.

Induction of Th17 Cellular Immunity With a Novel Nanoemulsion Adjuvant

"Th17 (T-helper-17) cytokine responses have been recently recognized as an important component for the protective immunity produced by vaccination. However, the mechanism by which immune adjuvants induce Th17 immunity has not been defined.........While the function of Th1 and Th2 cells is well documented, the newly recognized subset of Th17 cells produce interleukin (IL)-17A, IL-17F, and IL-22; however, its function is not entirely clear.1 Although IL-17 was initially found to play an important role in inflammation and autoimmunity, more recently it has been shown to be important in protective immune responses induced by vaccinations.2,3 While it is known that IL-17 induction requires IL-6, TGF-β (transforming growth factor-beta), and IL-23 to establish a persistent Th17 cell population (at least in mice), the role adjuvants play in the enhancing Th17 immunity has not been well studied."

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2860868/

The article on Vaccine DNA effect.

An Unexpected Actor in Vaccination: Our Own DNA

"The teams of Doctor Christophe Desmet and Professor Fabrice Bureau, of the Laboratory of Cellular and Molecular Physiology within the University of Liège's GIGA-Research centre, and of Professor Ken Ishii at the University of Osaka in Japan have just discovered an unexpected mode of action for the vaccine adjuvant alum. When a vaccine containing alum is injected, contact with alum apparently pushes certain cells of the body to release their own DNA.
The presence of this DNA outside the cells, a place where it is not to be found in normal conditions, thus acts as a stimulant of the immune system and strongly boosts the response to the vaccine. .....Developed in the middle of the 20th century, alum has largely demonstrated its effectiveness and safety of use. That it is why it is found in numerous vaccines. Tens of millions of doses of alum are thus administered each year, and each person in our Western societies has probably received alum at least once in their life. Nevertheless, alum was developed in a relatively empirical manner; the way it helps the immune system to respond to vaccines had not been properly understood up until now."

http://www.sciencedaily.com/releases/2011/07/110717204910.htm

They may understand more about the way it causes the immune system to respond to vaccines, but they don't say anything about what effecting DNA release may do. I have read DNA release occurs during some chronic disease conditions, exposure to UV radiation, and happens relative to aging. It says "contact with alum apparently pushes certain cells of the body to release their own DNA". I wonder which ones?

I intend to follow up on telomeres DNA damage and release for any who might happen to still be visiting this, by now, obscure thread.

While I have had this post typed out for a few days I had not decided to submit it, but since then the new gene and enviromental flare up has appeared, so I am posting. The following two articles particularly prompted me to share some thoughts.

Environment, not just genetics, at play in autism

http://news.yahoo.com/environment-not-just-genetics-play-autism-211331709.html

Autism linked to hundreds of genetic mutations

http://articles.latimes.com/2011/jun/09/health/la-he-autism-20110609

A few thoughts I had before reading these two articles.

The info on mutations labels them sponataneous as opposed to induced. Can they always know if a mutation is sponateous or induced? It also appears that what is called "spontaneous" mutations are not always the result of "chance", at least by the things I have read. How can they be sure that what is called spontaneous is truly spontaneous? Do spontaneous mutation rates vary between individuals? It seems possible that much of what are called spontaneous mutations are caused by enviromental factors of some nature. This would make them induced. If sponataneous mutation rates vary at all over time then they are not truly spontaneous, but outcomes based on malleable factors. Why isn't it logical to think that whatever machinery that produces dna replication is subject to external forces or feeedback just like any other system? It may just appear as spontaneous. If they believe that pre-pregnancy and first trimester folate supplementation reduces autism rates{which I imagine is true} and they think that at times spontaneous mutations are involved with autism rates it is reasonable to ask if increased folate reduces spontaneous mutations. If it does, this would seem to cast spontaneous mutations in a strange light. It could be that the two are not directly related, but some synergy of insult caused malfunction is involved in some cases. I am only thinking about these matters, not saying I have a belief about the effect of mutations and I have not read that they are found in the majority of thoses tested who have autism. But, it does seem there is too much to it to dismiss and do believe most who have autism are simply more genteically susceptible to autism then others. This doesn't mean that there is often a genetic defect, but the enviromental confluence of factors effects them more than others producing a varying degree of dysfunction with some more immune related than others depending how an antigenic response profile develops in each child. Also, there maybe a component in addition that is involved at a certain time such as inflamtion due to infection or virus that accompanies the risk factors that many more children have, but don't have this additional component that pushes them into a high suscepibility state where vacccines, illlness, allergic conditions , food reactions, antibiotics, drugs, or bacteria/fungal dsybiosis and systemic bacterial effects, additional viruses, push them over alone or in combination and more easily and into varying severity due to the now delcate balance of a number of critical sytems. This would be like one with both immune defficiencies and over reactivity except the immune system is tied to endocrine, hormonal, and neurotransmitter and notably some organ function like the gut and brain, and others indirectly like the pancreas, liver, and kidney and probaly all at some level. I think benezene/phenol,concentrated amines/amides, and aromatic compounds of all sorts like benzoates are strongly involved in this. These are common chemicals in antidepressants that would effect the carboxylacetylation, and sulfations and other systems as do Tylenol, antihistamines, and other drugs. Diphenhydramine has properties like some SSRI's. So, it maybe be the increased indiscriminate use of these substances along with bacterial populations that flourish in a phenol laden enviroment in and oustide the body that change gut ecology and deplete sulfate, as say Tylenol does, which also increases candida populations. That is maybe why Benzene from auto exhaust heaviest around freeways might increrase autism prevalence while not causing it by any means alone. Studies suggest spring births acount for higher levels of autism and the flu season and increased cold and flu medicines, tylenol, and anti-biotics would likely be taken more in pregnancies as the gestational period would run through this season. Also, jaundice has been reported at higher rates in newborns who later are diagnosed with autism. This could relate to the overload of these coumponds and deplete detox and Cytochrome P450 showing as jaundice. My wife's mother was diagnosed with TB and later determined only to be a carrier and later testing said she did not have it at all though early on in around 1957 was treated with 3 drugs that appear to bear on all of this. She said they gave her two drugs and a shot which must have been Pas, Isoniazid, and Streptomycin. Isoniazid has antidepressant properties. How this relates to my wife's problems is not clear as she was born some years later. But, I don't know if her mother continued on these drugs for a prolonged period. If not, it may still have had an effect on her mothers system that persisted.

"Isoniazid (Laniazid, Nydrazid), also known as isonicotinylhydrazine (INH), is an organic compound that is the first-line antituberculosis medication in prevention and treatment. It was first discovered in 1912, and later in 1951 it was found to be effective against tuberculosis. Isoniazid is never used on its own to treat active tuberculosis because resistance quickly develops. Isoniazid also has an antidepressant effect, and it was one of the first antidepressants discovered. ...Isoniazid inhibits the P450 system. ... Peripheral neuropathy and CNS effects are associated with the use of isoniazid and are due to pyridoxine (vitamin B6) depletion "

http://en.wikipedia.org/wiki/Isoniazid

PAS
"4-aminosalicylic acid, commonly known as PAS, is an antibiotic used to treat tuberculosis. This organic compound has been use since the 1940s for the treatment of inflammatory bowel diseases (IBDs), where it has shown greater potency in ulcerative colitis and Crohn's disease. It is thought to act via NF-κB (nuclear factor-kappa B) inhibition and free radical scavenging. 5-Aminosalicylic acid, sold under the name mesalazine, is a closely related compound that also has medical uses.

Pharmacology

With heat, aminosalicylic acid is decarboxylated to produce CO2 and 3-aminophenol.

The U.S. FDA assigned PAS to pregnancy category C, indicating that it is not known whether it will harm an unborn baby.

Side effects

Gastrointestinal side-effects (nausea, vomiting, diarrhoea) are common; the delayed-release formulation is meant to help overcome this problem. It is also a cause of drug-induced hepatitis. Patients with glucose-6-phosphate dehydrogenase deficiency should avoid taking aminosalicylic acid as it causes haemolysis. Thyroid goitre is also a side-effect because aminosalicylic acid inhibits the synthesis of thyroid hormones. Drug interactions include elevated phenytoin levels. When taken with rifampicin, the levels of rifampicin in the blood fall by about half.[5]

[History

PAS was discovered by the Swedish chemist Jörgen Lehmann upon the report that the tuberculosis bacterium avidly metabolized salicylic acid. Lehmann first tried PAS as an oral TB therapy late in 1944. The first patient made a dramatic recovery. The drug proved better than streptomycin, which had nerve toxicity and to which TB could easily develop resistance. Late in the 1940s, researchers at Britain's Medical Research Council demonstrated that combined treatment with streptomycin and PAS was superior to either drug alone. Aminosalicylic acid is sold in the U.S. by Jacobus Pharmaceutical as Paser.

Synthesis

PAS is manufactured by the carboxylation of 3-aminophenol."


http://en.wikipedia.org/wiki/Para-aminosalicylic_acid

CLINICAL IMPLICATIONS OF ISONIAZID, PAS ANDSTREPTOMYCIN BLOOD LEVELS INPULMONARY TUBERCULOSIS

"The metabolic products of INH in humans have been determined byurinary excretion studies; they are isonicotinic acid, hydrazones, INHconjugates, acetyl-INH, some unidentified amines and the free drug.9 Ofthese, only the free unmetabolized INH has microbiologic activity. It hasbeen shown in vitro'0 and in ViVo6, 11 that PAS will compete with INH forthe acetylating capacity of the host. As a consequence, PAS will some-times, but not always, cause an elevation of the levels of free INH in in-dividuals. Other aromatic amines such as the sulfa drugs and PABA mayhave the same effect, and apparently by the same mechanism.7 The chemi-cal measurement of free INH and its metabolites is difficult and uncertainin serum; as a consequence,microbiologic assay remains the method ofchoice to date for determining free INH. It is hoped that chemical studiesof rates of inactivation of PAS, PABA or sulfa may prove to parallel INHinactivation studies determined microbiologically and thus provide asimple practical test. This problem is complicated by the facts that thepredominate metabolic pathways for these drugs are as follows: acetyla-tion of INH, PAS, PABA and sulfa drugs in the liver, and glycine conju-gation of PABA in the liver and of PAS in the kidney.

Iproniazid (Marsilid't), the isopropyl derivative of INH, was essentiallydropped for antituberculous therapy in 1953-54 because of its high cere-bral toxicity. We have recently re-affirmed that it has an in vitro antitu-berculous effect of about one-half that of INH on an equimolar basis. Onthe other hand, it produces urine18 and serum'2 levels of free biologicallyactive IPH significantly hiigher than equimolar doses of INH in humans.Its favorable action in clinical tuberculosis can now be ascribed to itshydrazine molecule and to its additional action on several cerebral enzymesystems, including the mono-amine oxidase system."

Wiki states :"Precursor to pesticides and pharmaceuticals

Hydrazine is a useful building block in organic synthesis of pharmaceuticals and pesticides. One example is 3-amino-1,2,4-triazole and another is maleic hydrazide. The antitubercular drug isoniazid is prepared from hydrazine."


http://docs.google.com/viewer?a=v&q=cache:6xdbsDVEnEsJ:www.ncbi.nlm.nih.gov/pmc/articles/PMC2248973/pdf/tacca00122-0158.pdf+inh+pas&hl=en&gl=us&pid=bl&srcid=ADGEESixZmymnIOn7NXWk_0vBntvJqpk0KwDVAkxb7QFjbIbDIZwwIfFZGIBr0EV5eYTzjc6eWrQEmia2g2_dzK0idYljSnz410tZBnJmMvyaBnVX4To3zRipMW9lF98nNEZ1fWaeGbw&sig=AHIEtbSfCCczpYvWnlueDEvTRSPxskbx5w

Pharmacologic effects on mitochondrial function

http://onlinelibrary.wiley.com/doi/10.1002/ddrr.106/abstract

Newborn jaundice linked to autism
http://www.usatoday.com/yourlife/health/medical/autism/2010-10-11-autism11_ST_N.htm

Diphenhydramine - Wiki
“Diphenhydramine is histamine H1 receptor antagonist.[21] By blocking histamine in the capillaries it can reduce the intensity of allergic symptoms. Diphenhydramine crosses the blood-brain barrier(BBB) and antagonizes the H1 receptors centrally. Its effects on central H1 receptors causes drowsiness.[22]
Like several other first-generation antihistamines, diphenhydramine is also a potent competitive antagonist of muscarinic cholinergic receptors, and, as such, at high doses can cause anticholinergic syndrome.[23]
In the 1960s, diphenhydramine was found to inhibit reuptake of the neurotransmitter serotonin. This discovery led to a search for viable antidepressants with similar structures and fewer side-effects, culminating in the invention of fluoxetine (Prozac), a selective serotonin reuptake inhibitor (SSRI).[24][25] A similar search had previously led to the synthesis of the first SSRI, zimelidine, from brompheniramine, also an antihistamine.
Diphenhydramine also acts as a sodium channel blocker, which is responsible for its actions as a local anesthetic.[
http://en.wikipedia.org/wiki/Diphenhydramine

Sodium benzoate
“Professor Peter W. Piper of the University of Sheffield claims that sodium benzoate by itself can damage and inactivate vital parts of DNA in a cell's mitochondria. Mitochondria consume oxygen to generate ATP, the body's energy currency. If they are damaged due to disease, the cell malfunctions and may enter apoptosis. There are many illnesses now tied to DNA damage, including Parkinson's and other neurodegenerative diseases, but above all, the aging process in general.”

http://en.wikipedia.org/wiki/Sodium_benzoate

The Cerebral Cortex appeared a very prominent factor to me as I had posted on it earlier in this thread and this paints consistent picture, at least regarding my wife, with most things, if not all of the things, mentioned in this thread. Neuronal communication and protein functioning are also a strong factors in this region. The article linked to below makes a very important point. The gene expression element allows for the idea that there is something effecting gene expression as a causative factor. Of course it may be a mixture of intrinsic gene numbers and altered expression or mainly one or the other depending on the case.

Autism Changes Molecular Structure of the Brain: Discovery Points to a Common Cause for Multifaceted Disease

http://www.sciencedaily.com/releases/2011/05/110525131701.htm

"If you randomly pick 20 people with autism, the cause of each person's disease will be unique," said principal investigator Dr. Daniel Geschwind, the Gordon and Virginia MacDonald Distinguished Chair in Human Genetics and a professor of neurology and psychiatry at the David Geffen School of Medicine at UCLA. "Yet when we examined how genes and proteins interact in autistic people's brains, we saw well-defined shared patterns. This common thread could hold the key to pinpointing the disorder's origins."

The research team, led by Geschwind, included scientists from the University of Toronto and King's College London. They compared brain tissue samples obtained after death from 19 autism patients and 17 healthy volunteers. After profiling three brain areas previously linked to autism, the group zeroed in on the cerebral cortex, the most evolved part of the human brain.

The researchers focused on gene expression -- how a gene's DNA sequence is copied into RNA, which directs the synthesis of cellular molecules called proteins. Each protein is assigned a specific task by the gene to perform in the cell.

By measuring gene-expression levels in the cerebral cortex, the team uncovered consistent differences in how genes in autistic and healthy brains encode information.

"We were surprised to see similar gene expression patterns in most of the autistic brains we studied," said first author Irina Voineagu, a UCLA postdoctoral fellow in neurology. "From a molecular perspective, half of these brains shared a common genetic signature. Given autism's numerous causes, this was an unexpected and exciting finding."

The researchers' next step was to identify the common patterns. To do this, they looked at the cerebral cortex's frontal lobe, which plays a role in judgment, creativity, emotions and speech, and at its temporal lobes, which regulate hearing, language and the processing and interpreting of sounds.

When the scientists compared the frontal and temporal lobes in the healthy brains, they saw that more than 500 genes were expressed at different levels in the two regions.

In the autistic brains, these differences were virtually non-existent.

"In a healthy brain, hundreds of genes behave differently from region to region, and the frontal and temporal lobes are easy to tell apart," Geschwind said. "We didn't see this in the autistic brain. Instead, the frontal lobe closely resembles the temporal lobe. Most of the features that normally distinguish the two regions had disappeared."

Two other clear-cut patterns emerged when the scientists compared the autistic and healthy brains. First, the autistic brain showed a drop in the levels of genes responsible for neuron function and communication. Second, the autistic brain displayed a jump in the levels of genes involved in immune function and inflammatory response.

"Several of the genes that cropped up in these shared patterns were previously linked to autism," said Geschwind. "By demonstrating that this pathology is passed from the genes to the RNA to the cellular proteins, we provide evidence that the common molecular changes in neuron function and communication are a cause, not an effect, of the disease."

The next step will be for the research team to expand its search for the genetic and related causes of autism to other regions of the brain."

For the neurodiversity folks I would like to say that it is a noble and loving thing to desire to guard the dignity of people effected by autism no matter what the cause, but without even a seeming second thought the people producing the article refer to the cause or brain state odf those with the autism in view with the following notions.

"The discovery also identifies a new line of attack for researchers, who currently face a vast array of potential fronts for tackling the neurological disease and identifying its diverse causes."

"This common thread could hold the key to pinpointing the disorder's origins."

"For decades, autism researchers have faced a baffling riddle: how to unravel a disorder that leaves no known physical trace as it develops in the brain. Now a UCLA study is the first to reveal how the disorder makes its mark at the molecular level, resulting in an autistic brain that differs dramatically in structure from a healthy one."

Clarification: In the last post I wrote:
"It may be additional D3 , while helping with sulfation, additionally down regulates an already subdued VDR function and leads to greater pathogenic and immune suppression leading to autoimmunity at times as Dr. Trevor Marshall proposes."

I should have said simply additional vitamin D as in 25-D, not D3 as in 1-25D. In a reasonably healthy state Vitamin D {25-D}can downregulate the VDR, D3{1-25D} upregulates it. But,if chronic immune pathogens are involved then the 25D is converted to 1-25D and this according to Dr Marshall produces a damageing imummne response.

Metabolism of vitamin D and the Vitamin D Receptor

http://mpkb.org/home/pathogenesis/vitamind/metabolism

This thread started with the gut and bacteria and progressed though a number of effected systems related to immune function, neurotransmitters, toxins and many other things by extension, I have kind of come full circle back to the first crude picture of what I thought was happening in many cases of reggressive autism and similar or related syndromes with one novel exception. The exception is the inclusion of the involvement of the VDR{Vitamin D Receptor.
For me it was Dr. Rosemary Warings 1993 work that was pivitol in associating many other biological dysfunctions in my wife that mimicked what parents were saying about there autistic children's problems. I could not locate the original reference of her work, but the following is adequate to relate her findings."
"Dr. Rosemary Waring has demonstrated low levels of free sulfate in the plasma of autistic people. Free sulfate homeostasis is regulated by reabsorption in renal tubules primarily. Opioids change sodium, bicarbonate, and chloride reabsorption in the kidney, but no work has been done on sulfate reabsorption.

"Waring (1993) has demonstrated deficiencies in the sulphur-transferase capabilities of people with autism. This inadequacy is not the consequence of a missing enzyme (sulphur transferase) but of insufficient sulphate ions for the sulphation to be accomplished."

http://www.healing-arts.org/children/autism-overview.htm

I am dismayed that my focus on other medical problems I sought to understand, that to me are clearly linked back to what seem to be the biological problems that underlie the process, caused me to forget central parts of what could be causing the whole problem. The recent sulfate sidebar link posted on the AoA homepage reminded me of this factor. The article is here:

http://www.couriermail.com.au/ipad/sulfate-test-breakthrough-for-babies/story-fn6ck51p-1226051717005

This article led me to find another dealing with mercury and sulfate in Florida marshes linked here:

http://floridaindependent.com/27200/everglades-mercury-methylmercury-sulfate-runoff/

This made me wonder what was causing low sulfate levels in the children as Waring says the enzyme is present. It could be proposed gut problems and ecology of the the gut not producing the sulfate ios and mentioned in her work and that leads to asking why the gut is imbalanced. It could be a few things, or one or multiple factors in tandem depending on the case. The additon of looking at the VDR as possible bearing on sulfate levels may link the VDR as beazring strongly on sulfaste levels and mercury being involded in causing or worsening the problem.
If the VDR being bound disrupts pathogenic control and bears on gut ecology though inteation with the innate immune function and also eventually rthe adaptive immune funtions then the autoimmune elements in other medical conditons may be tied back to the VDR/sulfate/mercury and if we are right avaccine connection with or without mercury. This article, "Critical role of vitamin D in sulfate homeostasis: regulation of the sodium-sulfate cotransporter by 1,25-dihydroxyvitamin D3", might at first blush give credance to the idea of Vitamin D3 supplementation for sulfat problems, but if the VDR is bound then that alone could negatively effect sulfate levels.

http://ajpendo.physiology.org/content/287/4/E744.full

If you digested this article you may be ready to go get Vitamin D3, but it is possible that while sulfate levels may be helped by Vitamin D3 it seems probable to me that this does nothing to correct the underlying reason that VDR knockout mice had a problem with sulfate metabolism and that the likely co existing and causation of VDR disruption will not be dealt with by adding D3. It may be additional D3 , while helping with sulfation, additionally down regulates an already subdued VDR function and leads to greater pathogenic and immune suppression leading to autoimmunity at times as Dr. Trevor Marshall proposes.

Some may be more disposed to additional autoimmune and metabolic problems that manifest in various degrees. Some may be sub-acute, but in my wife's case I believe the bones spurs and pre-diabetic/insulin resistance and the begginings of Rheumatoid arthrits{and these are minor comapred to what happended to her brain}developed from the primary dysfunctions in immunity and sulfation involving mercury/ likely vaccines/ and the ppropogation of increasing damage by the pathogens she could not control due to immune alteration and also by the toxins, particularly in the gut, the organisms produced. There is mcuh, much more systemic dysfunction that could be discussed and some has been thougout this thread. But, those we reasonable familiarity with these issues can see the possible connection to the VDR/ Vitamin D/ and Sulfate levels not to mention calcium function in cells and all that entails. How much could polymorphisms be causing VDR problems if at all involved or is it mercury disrupting the immune system or viral interacitions? The chicken and egg or synergy scenarios are unresolved, so the question remains. Also, how much of these factors may exist they predispose a child to react badly to vaccines or are vaccines enough depending on certain genetic factors alone?
It may be all of the above.

I won't comment on the following links, but they give food for thought related to all of these matters.

Genetic background of lead and mercury metabolism in a group of medical students in Austria.

http://www.ncbi.nlm.nih.gov/pubmed/19515364

NaSi-1 and Sat-1: structure, function and transcriptional regulation of two genes encoding renal proximal tubular sulfate transporters.

http://www.ncbi.nlm.nih.gov/pubmed/15833267

Association of vitamin D receptor gene polymorphisms with childhood and adult asthma.

http://www.ncbi.nlm.nih.gov/pubmed/15282200

Allergies, Asthma May Play Role in Autism

http://www.webmd.com/brain/autism/news/20050207/allergies-asthma-may-play-role-in-autism

Factors affecting susceptibility and resistance to tuberculosis

http://thorax.bmj.com/content/56/suppl_2/ii23.extract

Mercury exposure in humans

http://www.articlesbase.com/health-articles/mercury-exposure-in-humans-1152865.html

Stanford researchers make scientific breakthrough

“My personal opinion is that the role of the immune system is crucial to the disease development. That would be the time when using an immune based approach could prevent the disease.”

http://voice.paly.net/node/27486

Helpful D Info
Vitamin D Council Glossary

http://www.vitamindcouncil.org/reference/glossary-V.shtml

Benedetta asked nearly a year ago:

"What does this mean?
Does this mean that they are going to use nicotinic acid and tryptophan to make a isomer of B12 that can be absorbed by a person with acquired mitochondrial disorder?"

The value of the substance discussed in the link below may be useful for the inflamation related to autism and brain effects in many autistics though it is not proposed as directly having a mitochondrial effect or even an application for autism, but time will tell whether this new isomer may have indirect effects on mitochondrial funtion. It is related strongly with scope of this whole thread though. Also, I don't see it as anywhere near a treatment with the ability to abate or reverse many of the biochemical amd metabolic aspects of those with biomedically related autism.

Star Scientific Has Home Run Potential

"Because of the astonishing success of the Star Scientific compound in encouraging new neuronal cell growth and reducing B-amyloid at the cellular level, Johns Hopkins University—a major research institution—is phasing in new uses of the compound in several other disease venues: cancers, thyroid, arthritis, and other diseases. Of note, research at the Johns Hopkins suggests that a low grade inflammation in pregnant women can pass through the placenta and blood-brain-barrier and cause aberrant neuronal growth within the fetal brain that could lead to autism and other disorders of presumed neurodevelopment origin, like schizophrenia and cerebral palsy.*


'On 2/9/2011 Star Scientific announced that the subject of its provisional patent application, a pure form of a single isomer of anatabine, could be administered to treat numerous disorders, including those with inflammatory components, aberrant immune response and/or inappropriate cell proliferation. The application indicates that the disorders which may be treated with this discovery include inflammation occurring in brain swelling or neurodegenerative disease such as Alzheimer's disease, multiple sclerosis, and Parkinson's disease. Star said: “This isomer can be administered in a composition containing a therapeutically effective dose of anatabine to treat chronic low-level inflammation."


Simple derivatives of pyridine

Via
Nicotinic acid → dihydronicotinic acid → 1,2-dihydropyridine [66]

one end product is:
anatabine


Nice that this popped up at this time for wher I have been researching.
Brain Cell Migration During Normal Development May Offer Insight on How Cancer Cells Spread

"During normal development cells divide, arrange themselves in appropriate patterns, and specialize to form discrete tissues and organs. For the body to develop properly, cells must coordinate their migratory patterns and the process by which they differentiate, or evolve from less-specialized cells into more-specialized cell types. A lack of such coordination leads to disordered development and, in some cases, cancer....

Jossin and Cooper set out to analyze how cells migrate in the cerebral cortex of the developing brain. The cerebral cortex, gray matter of the cerebrum, is the brain's command and control center where cognition and planning occur, and it is particularly well developed in humans.

The cerebral cortex is composed of horizontal layers of nerve cells, or neurons, which are specialized for different functions and connected vertically into circuits. If some neurons are in the wrong layers, the wiring can be defective and neurological disorders including epilepsy, autism and schizophrenia may result."

http://www.sciencedaily.com/releases/2011/04/110424152453.htm

Immunohistochemical detection of raf protein kinase in cerebral cortical areas of adult guinea pigs and rats
Not Studying People, but possibly bears on Raf Kinase in Humans
http://www.sciencedirect.com/science?_ob=ArticleURL&_udi=B6SYR-48363C7-344&_user=10&_coverDate=11%2F12%2F1993&_rdoc=1&_fmt=high&_orig=gateway&_origin=gateway&_sort=d&_docanchor=&view=c&_acct=C000050221&_version=1&_urlVersion=0&_userid=10&md5=e217e04c0af9cdc0985e8ac291624076&searchtype=a

Cerebral cortex

http://en.wikipedia.org/wiki/Cerebral_cortex

Angiotensin
I imagine Trevor Marahsll is aware of this, but either way Benicar may effect more than the VDR as a major effect.

http://books.google.com/books?id=H0cMhfEGvJgC&pg=PA154&lpg=PA154&dq=intracellular+signalling+of+neurons+raf-1&source=bl&ots=6nFvQS2ZqN&sig=ktG-HWvpZ1SjZENRCg2Npt-jg3c&hl=en&ei=xwqzTfqYE4OUtwevr9jpDg&sa=X&oi=book_result&ct=result&resnum=8&ved=0CEIQ6AEwBw#

Epigenetic instability of cytokine and transcription factor gene loci underlies plasticity of the T helper 17 cell lineage.

http://www.ncbi.nlm.nih.gov/pubmed/20471290

Decay-accelerating factor 1 (Daf1) deficiency exacerbates xenobiotic-induced autoimmunity.

http://www.ncbi.nlm.nih.gov/pubmed/20408894

Precarious Balance: Th17 Cells in Host Defense

"Consistent with the ability of fungal components to drive IL-17 production, some animal models of opportunistic fungal infections suggest a positive, and in some cases essential, role for Th17 cells. Neutralization of or deficiency in IL-23 or IL-17 during disseminated and oral candidiasis and pulmonary aspergillus, among others, exacerbates pathology characterized by inadequate neutrophil recruitment, increased fungal burden, and reduced chemokine and antimicrobial expression (13, 35, 77, 95). In support of these findings, reexposure to antigen drives IL-17 production by human memory T cells specific for C. albicans antigen (1, 93, 95). However, vaccination models of Ag-induced protection and infection by C. albicans in TRIF–/– mice have linked the Th17 lineage to deleterious inflammation rather than protective immunity and buttress the prior emphasis on the Th1 lineage for host defense (7, 18, 68). Several of the fungal antigens identified as nonprotective in vaccine drive DCs toward an alternative activation state characterized by IL-23 rather than IL-12 production, thus supporting the expansion of the Th17 (sometimes concomitantly with the Th2) lineage at the expense of the Th1 and Treg lineages (18). Such bias results in tissue injury and reduced fungal clearance, in part by impairing the killing activity while extending the viability of recruited neutrophils (8, 102). Furthermore, expansion of the Th17 subset establishes a positive feedback loop that favors the Th17 response (18, 102) and inhibits the induction of Tregs required for homeostatic tolerance to commensal but opportunistic fungal pathogens (6, 63)."

http://iai.asm.org/cgi/content/full/78/1/32

With this last article I am not suggesting than autism or other dieases states are accompanied with a diagnosed autoimmune polyendocrine syndrome. This syndorme is suggested to be due to innate genetic factors, yet it seems possible that a degree of dysfuntion of autoimmunity and endocrine problems could come about from the establishment of a mixture of chronic pathogenic problems and epigentic changes. My main reason for posting it is it addresses TH1 & 17 function relative to pathogens.

Increased IL-17A secretion in response to Candida
albicans in autoimmune polyendocrine syndrome type 1
and its animal model

http://onlinelibrary.wiley.com/doi/10.1002/eji.200939883/pdf

This article is not suprising, nor novel in the concepts it suppots. But, it does at least suggest the science is showing the posssiblities of strong gut interacctions which many in our community already knew. TH17 is named as a major player.

http://www.sciencedaily.com/releases/2011/04/110421141632.htm

Interleukin-17 induces rapid tyrosine phosphorylation and activation of raf-1 kinase in human monocytic progenitor cell line U937.

http://www.ncbi.nlm.nih.gov/pubmed/10334935

I have not put together a plausible schematic, but it seems possible that a possible effect of some vaccines is their effect on TH17/IL17 leading to many states including Autism. If IL 17 is involved in killing mucosal and other pathogens it seems at first to indicate that a lack of TH17/IL17 release would be the problem. But, it may be that it is a disorder of TH17/IL17 function. Due to not fully unserstanding the mechanism I propose that the idea that a property of a vaccinemight alter the funtion by altering the targets of TH17/IL17. That is, common fungi and some bacteria may be illiciting minor responses while other antigens are being targeted. This could mean IL 17 is actualyy overactive, but causing inflamation by reacting to the wrong proteins. If certain pathogens are still correctly targted while others not, autistic children would possibly have lower levels of certain bacteria and higher levels of other and possibly higher yeast loads.

Induction of Th17 Cellular Immunity With a Novel Nanoemulsion Adjuvant
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2860868/


Molecule That Destroys Bone Also Protects It, New Research Shows
http://www.medicalnewstoday.com/articles/70323.php

Children With Autism Have Fewer Cavities
http://gooddentalhealth.blogspot.com/2008/12/children-with-autism-have-fewer.html

Candida albicans Dampens Host Defense by Downregulating IL-17 Production

http://www.jimmunol.org/content/185/4/2450.abstract

Differential effects of IL-17 pathway in disseminated candidiasis

http://www.ncbi.nlm.nih.gov/pubmed/20160669

In case anyone is following this thread. I lied , my sabbatical will have to wait a bit. Not long after my last post I came across a find about Pentosidine levels in schizophrenics. Since my wife has some Rheumatoid Arthritis it triggered the connection between oxidative stees, cytokines ,and inflamation.

"Japanese researchers have discovered that about 40 percent of people suffering from schizophrenia show higher blood levels of the amino acid pentosidine than healthy people, findings that are expected to help doctors diagnose, prevent and treat the disease." "They discovered that in 21 of the 45 patients, blood levels of pentosidine were 1.7 times the level of healthy individuals on average. They also found that antipsychotic medications are likely to be less effective in patients with elevated pentosidine levels.

In 11 patients, levels of a vitamin B6 compound, which helps discharge pentosidine from the body, were one-fifth the level of healthy persons, according to the team. The vitamin B6 compound is being clinically tested in the United States as a treatment for complications from diabetes."

http://www.yomiuri.co.jp/dy/national/T100612001288.htm

"Pentosidine is a biomarker for advanced glycation endproducts, or AGEs. It is a well characterized and easily detected member of this large class of compounds.
Derived from ribose, a pentose, pentosidine forms fluorescent cross-links between the arginine and lysine residues in collagen."

http://en.wikipedia.org/wiki/Pentosidine

Ribose
"It is related to deoxyribose, as found in DNA. Once phosphorylated, ribose can become a subunit of ATP, NADH, and several other compounds that are critical to metabolism.
Once converted, D-ribose-5-phosphate is available for the manufacturing of the amino acids tryptophan and histidine, or for use in the pentose phosphate pathway. The absorption of D-ribose is 88-100% in the small intestines (up to 200mg/kg/hr)."

http://en.wikipedia.org/wiki/Ribose

From my earlier post- Abstract
"We have examined the integrity of J774 cell nitric oxide (NO) production and glutathione maintenance, whilst NADPH supply was compromised by inhibition of the pentose pathway with 6-aminonicotinamide. In resting cells 6-phosphogluconate accumulation began after 4 h and glutathione depletion after 24 h of 6-aminonicotinamide treatment. Cellular activation by lipopolysaccharide/interferon-λ decreased glutathione by ∼50% and synchronous 6-aminonicotinamide treatment exacerbated this to 31.2% of control."

http://www.sciencedirect.com/science?_ob=ArticleURL&_udi=B6T36-3TMXY8S-P&_user=10&_coverDate=08%2F28%2F1998&_rdoc=1&_fmt=high&_orig=search&_sort=d&_docanchor=&view=c&_acct=C000050221&_version=1&_urlVersion=0&_userid=10&md5=d4d9552ec55a328b3720989fe700d289

"The oxidative phase of the pentose phosphate pathway is the major source of NADPH in cells, producing approximately 60% of the NADPH required."

http://en.wikipedia.org/wiki/Nicotinamide_adenine_dinucleotide_phosphate

Glucose 6-phosphate
http://www.uic.edu/classes/phar/phar332/Clinical_Cases/vitamin%20cases/thiamin/ppp.gif

Increased concentrations of serum pentosidine in rheumatoid arthritis

http://www.clinchem.org/cgi/content/full/44/2/250

I am still trying to get a this all into a possible picture of the acetylcholine/nicotinic acid/niacin and urine profile connection. I am also trying to see the way this scenario may be invloved in producing scizophrenic, autistic, and possibly alzheimer's like memory issues in some people. The b6 connection in the first aricle sounds familiar to those who have used it for autism in their children.

I cannot find any information on whether maleylacetone or succinylacetonecould be the cause of acetone breath so it may be an insulin resistance related issue. I am going on a sabbatical from all of this for a while. Where there is hope.....

Thanks for explaining it further and in more detail.
I understand.

This urine metabolite and Methylmalonicacid urea info is fun to watch come into view.
It made me look at the acetone breath issue again.

"MAAI pathway is also used to breakdown tyrosine catabolites. If MAAI is depleted/inhibited, toxic concentrations of tryosine intermediates such as maleylacetone and succinylacetone accumulate."

http://www.thedcasite.com/dcaforum/DCForumID4/83.html


"Propionic acidemia: Deficiency of propionyl CoA carboxylase, the enzyme responsible for metabolizing propionic acid to methylmalonate, causes propionic acid accumulation.

Illness begins in the first days or weeks of life with poor feeding, vomiting, and respiratory distress due to profound anion gap metabolic acidosis, hypoglycemia, and hyperammonemia. Seizures may occur, and bone marrow suppression is common. Physiologic stresses may trigger recurrent attacks. Survivors may have tubular nephropathies, intellectual disability, and neurologic abnormalities. Propionic acidemia can also be seen as part of multiple carboxylase deficiency, biotin deficiency, or biotinidase deficiency.

Diagnosis is suggested by elevated levels of propionic acid metabolites, including methylcitrate and tiglate and their glycine conjugates in blood and urine, and confirmed by measuring propionyl CoA carboxylase activity in WBCs or cultured fibroblasts.

Acute treatment is with IV hydration (including high-dose dextrose) and nutrition; carnitine may be helpful. If these measures are insufficient, peritoneal dialysis or hemodialysis may be needed. Long-term treatment is dietary restriction of precursor amino acids and odd-chain fatty acids and possibly continuation of carnitine supplementation. A few patients respond to high-dose biotin because it is a cofactor for propionyl CoA and other carboxylases.

Methylmalonic acidemia: This disorder is caused by deficiency of methylmalonyl CoA mutase, which converts methylmalonyl CoA (a product of the propionyl CoA carboxylation) into succinyl CoA. Adenosylcobalamin, a metabolite of vitamin B12, is a cofactor; its deficiency also may cause methylmalonic acidemia (and also homocystinuria and megaloblastic anemia). Methylmalonic acid accumulates. Age of onset, clinical manifestations, and treatment are similar to those of propionic acidemia except that cobalamin, instead of biotin, may be helpful for some patients.

http://www.merck.com/mmpe/sec19/ch296/ch296c.html

Benedetta,
There various strains of clostridia. Some may exist as part of the gut flora without problems. There are different antigenic specficities in different strains like a a or c and botulism has 7 specificities. I am not sure if other clostrida then the ones mentioned in our thread could be involved. On our farm we dealt with black leg. The report on autism and Clostridium histolyticum imples an ongoing colonization by that strain. This was not causing them to be hospitalized yet was in there gut. I believe you said you are in Ky somewhere in a past thread. That is my native state although I no longer live there.

http://jmm.sgmjournals.org/cgi/content/full/54/10/987

http://www.ncbi.nlm.nih.gov/pubmed/9881820

Benedetta,

I agree I do not think that it is in my pancreas, but in the gut clostridia may possibly elicit an immune respone towards the pancreas. It may also relase a toxin that could effect the pancreas. I was in the hospital with attacks and have had some severe ones without being hospitalized.

http://jcp.bmj.com/content/49/6/500.abstract

I am proposing that an immune response to the clostridia or it's toxin or aberrant response immunally to it in the gut is damaging the pancreas.

http://gut.bmj.com/content/50/4/535.abstract

Nick, unlike your sister I am not a nurse practioner, I am a nothing.

But I have seen young cattle die of black leg. I cannot imagine such a bacteria that causes gas gangrene to be gentle enough to be in the pancreas making you just a little sick.

A young healthy cow one day and the next eyes clouded over, limping, fast becoming worse -bloating and death - all in hours - short hours.

My sister is a nurse practitioner and was asking her what was the best drug to eradicate clostridium histolyticum as I thought I may have it and it could be related to my pancreatic problems and IBS. Here is the dialogue.

Nancy,

I, as usual, am not sure of what the full connection might be. You are very likely correct that I don’t have this type of clostridia in my pancreas. Yet, I noted Ramona had clostridia in her years ago. I think I was exposed to this clostridia in a way hat elevated their numbers in my gut, and I am sure I got yeast problems from her although the yeast is not the issue here. I have read that this strain is found in the gut and may be related to autism. Any way I found taking the Enhansa relieved some of the discomfort and wondered if the reduction in cytokines was the reason as it is in the Enhansa helping Ramona’s issues. Please take a look at the two articles below. They show a plausible connection between cytokines and pancreatitis. So, I am thinking my pancreas may be suffering from an immune caused inflammation caused by the clostridia in the ileum or other area.


“The researchers also noted that children with autism had higher numbers of Clostridium histolyticum bacteria in their fecal microbiota. Their siblings also showed elevated numbers of this group of bacteria, although they were not as high as those found in autistic individuals, leading the researchers to speculate that gut microbiota may potentially play a role in the development of the disorder.”

http://www.pediatricsupersite.com/view.aspx?rid=65343


“Factors that may influence PSC activation during pancreatic necroinflammation include cytokines known to be important in the pathogenesis of acute pancreatitis, such as tumour necrosis factor α (TNF-α), and the interleukins 1, 6, and 10 (IL-1, IL-6, and IL-10).”


http://gut.bmj.com/content/50/4/535.abstract

Nick


From: nancy
Sent: Wednesday, June 09, 2010 6:18 AM
To: Nick Subject: Re: My Pancreas

Dear Nick,

It is very unlikely that you have this organisim. It is a gas producing organism that is usually fatal as it causes gas gangrene. It causes bubbles to form in the tissues and as these rupture gas is released and more bubbles form causing widespread tissue distruction as it goes. It isn't usually subtle or gradual. It is difficult to kill because it is anerobic and requires IV vancomycin. Oral dosing will not work on organ or soft tissue infections like it will in the intestinal tract for clostridia difficile. Pancreatitis is usually the autolysis of the pancreas by its own enzymes that become trapped within itself and cannot get out. Infection from enteric bacteria can result but highly unlikely this one.

Love, Nancy

--- On Tue, 6/8/10, Nick wrote:


From: Nick Subject: My Pancreas

Date: Tuesday, June 8, 2010, 6:23 PM

Nancy,

This is what I think is causing my pancreatic problems and my bowel issues. What should I take to kill this bacterium?


http://www.yourdictionary.com/medical/clostridium-histolyticum

Nick


This is a long read, and many may dismiss it, but it did seem to have a lot of validity in from what I saw.

http://www.arthritistrust.org/Articles/Candidiasis%20Scourge%20of%20Arthritics/index.htm

Benedetta,
I am have been looking at the vitamin D issue for a long time. Your thoughts seem to support Vitamin D as a positive in immune function. I am not sure what was going on with you and Vitmain D, but Ramona was put on high doses odf D by her doctor atwo or three years ago and she started to get worse. I took her off the high dose about 10 months ago although she took a multi that had it until about one or two months ago. She had aconstant battle with yeast and it was not seasonal. I am glad you seemed to resolve your problems.

Nick;
This I do know I had a yeast infection when I was carrying my son. It was winter. Winter has a lot of do with it too.

A few years ago I began to get a yeast infection every fall and kept it all winter. I am outside a lot in the summer - with farms and gardening.

I started taking vitamin D in the fall, and my yeast infection that I had at the time went away????!!!!! I have not had one since and that has been at least four years now.

Oh, except for the fourth day into the Atkin's diet. Dr. Atkins said in his book that this is common, and he did not know why. He had a theory: People on the low fat diet are not use to eating aged cheeses, which is a no - no on the low fat diet, thus our bodies have an allergric reaction to the dead yeast in the cheese.

My theory is: It really was a yeast infection, but what is really strange is that it affected us not in just the usual way, but also it affected (hurt) every - muscle and joint in our bodies. It did go away, and we have not had one since.

The acetone breath I mentioned may have been the Candida and the way her metabolism {map kinase} was effected due to effects in her pancreas.

Candida produces both Ethanol and Acetaldehyde.

http://journals.lww.com/pancreasjournal/Abstract/2003/08000/Pancreatic_Stellate_Cell_Activation_by_Ethanol_and.8.aspx

I have idiopathic pancreatits which I developed a number of years after I met Ramona and also started having yeast issues. I likely ended up with more
Clostridium histolyticum from her. All this probaly led to my IBS and the intestinal problems coffee gives me due to TNF and IL-10 reactions I could have started having. Enhansa gave me some relief too.

http://gut.bmj.com/content/50/4/535.abstract

Clostridium histolyticum - This has been known about, but they are just now making some connection with autism it seems.

"The researchers also noted that children with autism had higher numbers of Clostridium histolyticum bacteria in their fecal microbiota. Their siblings also showed elevated numbers of this group of bacteria, although they were not as high as those found in autistic individuals, leading the researchers to speculate that gut microbiota may potentially play a role in the development of the disorder."

http://www.pediatricsupersite.com/view.aspx?rid=65343

NMDA Receptor - kynurenic acid - glutamatergic signaling

http://www.ncbi.nlm.nih.gov/pubmed/18655201

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