Dr. Wakefield Sues Brian Deer and BMJ's Fiona Godlee
That’s My Boy!

The Inflammation Highway: aka Autism

  Tummy-ache-abdominal-pain-t13513By Lisa Goes




Lisa Goes is Contributing Editor to Age of Autism.


susan welch

Visitor, thanks for the video links. They were both appropriate and enjoyable.

Sorry you appear to be feeling so 'down'. You are right about the powerful, but we have the truth.

Hang in there.


from one small voice that has linked to the ":Atlantic", let me me state without qualification the Atlantic is a rag publication that deserves no respect and should be seen as a scumbag piece of journalism. I am ashamed to have ever linked one article of their putrid verbosity.


People without autism.



No money , No status, just truth. It will matter little.



II am only one, but I have innocently investigated it all. There is no meaning. Chaos rules. You can find effect continuously. When you seek to the end it all means shit. There is no meaning and I wished there was. The strongest rule. The ,most selfish rule.


The ACE2/Angiotensin, Rage TLR's and other aspects including HMGB1. This makes you think about latent viral expression in some with Autism and aspects o vascular effects in vascular constriction and dementia and also in Kawasaki's. Hypoxia diminishes antiviral immune responses. It seems to be a microcosm of how a vaccine may mediate a damaging inflammatory state in those predisposed and Covid may be doing this some with particular states of ACE2, maybe down regulated ACE2. II on't attempt to re-state all that is spoken about in this thread regarding these matters, but it is there.

HMGB1: A Possible Crucial Therapeutic Target for COVID-19?

High mobility group box-1 (HMGB1) is a chromatin-linked, nonhistomic, small protein with cytokine activity that has nuclear, cytosolic, and extracellular actions. It binds to chromosomal DNA but also to Toll-like receptor 3 (TLR3), TLR4, and the receptor for advanced glycation end products (RAGE) that activates nuclear factor (NF)-κB (Fig. 1a), which mediate the upregulation of leukocyte adhesion molecules as well as the production of proinflammatory cytokines and angiogenic factors that promote inflammation. HMGB1 was initially known as alarmin and is a well-recognized damage-associated molecular pattern (DAMP) protein.

Fig. 1.
a HMGB1 shows both intracellular and extracellular effects. By binding to TLR2, TLR4, and RAGE, it activates NF-κB which leads to the production of proinflammatory cytokines that have local and systemic effects. b HMGB1 is increased both locally and in the circulation in conditions like obesity, cystic fibrosis, and polycystic ovary, and, whenever insulin resistance occurs, it is produced by adipose tissue and the immune system. CFTR malfunction causes an increase in HMGB1, besides other changes such as inflammation and increased autophagy.


In our case my wife had re-occurring bronchial infections which were often viral. These declined progressively with many treatments along with eventually Olmesartan, which does numerous things in cell and immune system.

Doctor offers coronavirus protection advice

"Antihypertensives, a class called ARBs (angiotensin receptor blockers), which are normally used to reduce blood pressure and protect kidney function. ARBs increase ACE-2 activity and have been proposed as a treatment to promote healing of the lung in corona virus pneumonia. A recent study from China demonstrated through indirect measures that ACE-2 function declines with viral load and severity of COVID-19 pneumonia. For people already taking blood pressure medication, the inclusion of an ARB may improve the response to COVID-19 infection. The Federal government is sponsoring a trial of the ARB losartan for amelioration of COVID-19. However, the ARB that most enhances ACE-2 levels in humans is olmesartan (Benicar). Of all the ARBs, olmesartan has the greatest impact on immune function. "



On the topic of measles and atopic dermatitis there are conflicting reports, but this one suggests a timing that does associate with the start of measles virus vaccines. Again, many with autism don't show AD, but the terrain of their skin still may reflect aberrant function.

Atopic dermatitis is increased following vaccination for measles, mumps and rubella or measles infection.


COVID-19 may be tied to rare syndrome in children, UK doctors warn

Also, I know AoA is aware of this news, but given the detoxification and inflammatory effecting the systems of many with autism and the viral associations it is interesting to read the elements that they describe the condition with. {Toxic shock- Kawasaki's...fits with factors of this thread}

"The alert noted that these cases showed symptoms similar to those found in two rare conditions: toxic shock syndrome and Kawasaki disease. Toxic shock syndrome is a life-threatening condition that's caused by toxins produced by certain types of bacteria; Kawasaki disease is a childhood illness that causes inflammation in blood vessel walls, and in serious cases can cause heart damage."



Not too far back in this thread you will find information on ccr4/ccl17 and findings relating it to autism and showing effects in the brain. I am still working on this and how this could be related to atopic dermatitis which is much higher in those with autism. CCl17 is also related to "Dress Syndrome" and shows hypersensitivity. This possibly could be a trigger after MMR though I have not begun looking as to how this keratinocyte/skin reaction might communicate or effect the same factors in the brain. In the hypersensitive this could conceivably be a trigger and though many more may get atopic dermatitis without having autism there may be a correlation to study as to the age or degree one has the Atopic condition. There are many questions that could prove to abolish this theory, and MMR might only effect a subset in sparking regression or developmental effects or ADHD with or without Atopic Dermatitis. The first masles vaccine did not come till 1963 I have read, but certain flu vaccine among others began in wWorld Wae 2.
The first paragraph might show a timing relationship with Autism.

Two Pivotal Chemokines in
Atopic Dermatitis
Christian Vestergaard
"The incidence of atopic dermatitis has been rising in the wes
tern countries since World War II (2), a fact which has been
ascribed to better living conditions and the western lifestyle
(3, 4) although it seems to have levelled out during the 90’s
(5). Atopic dermatitis affects between 15% and 20% of all
Danish children (6, 7) however; the number varies with a li
fetime prevalence between 13% and 37% (8). In a Norwegian
study 13% of the population under the age of 20 was affected
by atopic dermatitis, whereas only 2% of the population over
the age of 20 was affected (9). In 60% of the cases the onset of the disease is in the first year of life
and in 85% of the cases before the age 5 years (10)."

"Infections also play a role in the pathogenesis of atopic
dermatitis. In a recent study it was shown that children who
were subjected to the measles, mumbs and rubella vaccination
or measles infectionhad a significantly higher risk of developing atopi dermatitis
ping atopic dermatitis than children who were not vaccinated or had had measles."



I t does not matter what i post anymore than the one reading this can be understood by another. I have understood another. That is of note..

Now here I go again, I see the crystal visions
I keep my visions to myself, it's only me
Who wants to wrap around your dreams and,
Have you any dreams you'd like to sell?
Dreams of loneliness,
Like a heartbeat, drives you mad
In the stillness of remembering, what you had,
And what you lost and what you had and what you lost


I keep my visions to myself. I have shared the science the reality would never be believed thoug I have alluded to it.


"You have done so very much on all of this, it is staggering piece of work"
After over a hundred thousand studies I am a puddle.
Nihilism. or Faith. I have not fared well in the milieu. over the last 23 years. I have been focused like a laser and am totally taxed in my ability at every turn. The vacillation between the two is a bit unhealthy.{understatement}. I want a n end point, but it just keeps unfolding. What is a post without a song?



Isaiah 9:6-7 ESV

So at his second coming he will be in control of government. No more humans just out for themselves, but instead really working for the good of us all. That is the future of mankind.

It is True - So Be It


Your last study you shared toward the end was about intestinal mucosal . After my son's third DPT reaction about a week later -- he filled his diaper with mucous, so I know what that looks like and now I know maybe why. Thanks.

Advent last Sunday and I was looking for a verse to share with my family about "Hope" That is the theme of the first Sunday of December.

Isaiah 9:6-7 ESV



Crucial role of NLRP3 inflammasome in a murine model of Kawasaki disease.


Kawasaki disease (KD) is a systemic febrile syndrome during childhood that is characterized by coronary arteritis. The etiopathogenesis of KD remains to be elucidated. NLRP3 inflammasome is a large multiprotein complex that plays a key role in IL-1β-driven sterile inflammatory diseases. In the present study, we investigated the role of NLRP3 inflammasome in a murine model of KD induced by Candida albicans water-soluble fraction (CAWS) and found that NLRP3 inflammasome is required for the development of CAWS-induced vasculitis. CAWS administration induced IL-1β production, caspase-1 activation, leukocyte infiltration, and fibrotic changes in the aortic root and coronary arteries, which were significantly inhibited by a deficiency of IL-1β, NLRP3, and ASC. In vitro experiments showed that among cardiac resident cells, macrophages, but not endothelial cells or fibroblasts, expressed Dectin-2, but did not produce IL-1β in response to CAWS. In contrast, CAWS induced caspase-1 activation and IL-1β production in bone marrow-derived dendritic cells (BMDCs), which were inhibited by a specific caspase-1 inhibitor and a deficiency of NLRP3, ASC, and caspase-1. CAWS induced NLRP3 and pro-IL-1β expression through a Dectin-2/Syk/JNK/NF-κB pathway, and caspase-1 activation and cleavage of pro-IL-1β through Dectin-2/Syk/JNK-mediated mitochondrial ROS generation, indicating that CAWS induces the priming and activation of NLRP3 inflammasome in BMDCs. These findings provide new insights into the pathogenesis of KD vasculitis, and suggest that NLRP3 inflammasome may be a potential therapeutic target for KD.


miR-155 Regulates claudin1 Expression in Humans With Intestinal Mucosa Dysfunction After Brain Injury.


Patients with craniocerebral trauma often have intestinal mucosal dysfunction, and the claudin1 protein plays an important role in intestinal mucosal function. Our previous work has shown that the expression of microRNA-155 (miR-155) in the peripheral blood of patients with craniocerebral trauma is decreased. Animal experiments also suggest that the expression of miR-155 is increased in the intestinal mucosa of mice with brain injury and the expression of claudin1 is decreased. We recruited 56 samples (35 patients with traumatic brain injury [TBI] and 21 patients without history of head trauma) to detect the expression of miR-155 on claudin1 regulation by quantitative polymerase chain reaction, reverse transcriptase polymerase chain reaction, and so on. We also used the receiver operating characteristic curve (ROC) to further evaluate the diagnostic value of the 2 biomarkers. From the results, we found that the expression level of miR-155 and claudin1 in the case group was lower than that in the control group. Human miR-155 (Hsa-miR-155) may positively regulate intestinal mucosal function by inhibiting the expression of claudin1, leading to intestinal mucosal barrier dysfunction. Combining the ROC curve data, the results further prove that miR-155 and claudin1 might be the new clinical diagnostic markers and treatment targets for the intestinal mucosal barrier dysfunction after TBI.


Trying to be cute with the bless you and ___ a couple of post back relating to some want to abuse you from "Sweet Dreams", but I was not in a right frame of mind to make any intelligent remarks at that time. Sorry.


Jenny said on June 27, 2015. "I appreciate it, too, Visitor. I'm just not as fast at absorbing and processing it all as you are. " I don't know anyone else who has either and I wish this was not the case. My family ostracized me in these matters early on so I have to eat it all and try to interact with them as though as I am a total ignoramus.

I realize I have been way way ahead of the curve. Do I need to apologize for this? I wish my family had a clue. I don't like conde3scending to others, but in this case I have no choice.


Culture is in Control


If there is a home I want to go there now. I cannot get through to anyone. Let it be over.


Sweet Dreams behind a cigarette.


And I'm talking to myself at night
Because I can't forget
Back and forth through my mind
Behind a cigarette
And the message coming from my eyes
Says leave it alone


The Police video a few posts began with a cigarette. I posted Sweet Dreams right after that. he rei9s on with the lyrics. I am hoping some have some phycological training to understand these posts. I poste sweet dramas right after. The lyric for White Stripe + Sweet dreams.





See the cigarette in every in Every Breath You Take posted earlier.




Tring to receive.


Benedetta, God is with us. There is only one thing I remain confident in. It is God is good all of the time. I trust His goodness and love. God has taught so much, but I am incredibly slow in understanding , and His patience is endless. Bless the Lord for Jesus, He is our blessed shepherd. Who could give Jesus proper glory? I have tried to love my wife as Christ loved the church. I will have to wait till I cross over to understand. At this point I find great beauty in the liberal mind and equally so in the conservative mind. I lean a bit to the right. That is how God made me. Life would not be worth living without the liberal mind and the same is true for life without the conservative love and life promoting freedom.
At the fringes the mind needs the conservative to preserve being. The liberal is needed to prevent narcissism and the divorce from self.. I find while liberalism teaches the most in this changing world it is the eternal unchanging truth of God that we will glory in through eternity. On the cross our confusion and answer lie. The cross is everything and glory. The Cross is God's one word response to or being. W are all related. Fuck you and bless you. I mean it.




Nick, sorry. Please ignore the repeat. Too late at night and I did some thing of a copy, paste and mess up!
The article is a great article too.

Barbara Fisher in her speech on the V.I.E. also continues to beat the drum that it is inflammation, and it is serious stuff.


Thank you Visitor:
I am caring for my 90 and 95 year old parents as well as my family. So I am tired most of the time, and short on time all the time.
It scares me about the Kawasaki's disease. What will it lead to on down the line?

My daughter is working toward a stroke or heart attack. She smokes, on birth control pills (because her hormones do not function correctly since she was 14 years old) She will soon be 39. She was a thin little thing all through college and then gained lots of weight in only one year - 100 pounds or more I think and even developed a buffalo hump. It has to do again with hormones, and the immune system and inflammation.. She has exercised it off, she does walk every day for miles.

I do the gluten free, very little milk except in cooking, I for myself do not eat gluten cause I found for my own self that it hurts my legs and feet. I do not eat peanuts cause it breaks me out, and that is also inflammation. .
Do you know what it takes to just get gluten out of your kitchen, and still cook something?
And getting peanut butter out of my kitchen makes me a food Nazis and apparently is harder than taking bread away from them. They all want their carbs.

We all try to fast. We are suppose to stop eating at six and wait as long as possible in the morning. Fasting I think helps reduce inflammation? Perhaps our bodies have to have so much carbohydrates to make glucose to use as energy to make immune cells? I

One of your links turned up to mention alcoholics -- I never have drank alcohol; I have seen some of my cousins actually die, and other cousins lucky enough to go prison instead of dying because of their addition to alcohol, or drugs,or really both. I don't know if my family history has a lot of alcoholics any more that the rest of the population? But this addiction stuff I think is all associated with pain from inflammation.

My husband was given opioids, lots of them; all nice ahd legal. That caused a crisis in the family as well as coming close to killing him.

Inflammation hurts. It hurts your feet, and legs, everywhere. It can cause people to seek out pain killers that gets us to addition.

A psychologist that treated my daughter six years ago, yeah, she was self medicating with some things that she did not need to be messing with. It was a long episode of events of a lot of health problems following a DPT vaccine (stupid, stupid, stupid), and she got caught right out off the bat when she did that. Anyway this psychologist treats all the unfortunate addicted doctors and nurses, and apparently there are a lot of them ; but he responded to my daughter's complaint that she just hurts all over; that yeah, he too is a recovering addict, and he too hurts all over, but being sober and hurting is better than not. He suggested that she walk and exercise a lot. Which she does.

There are no grand children and there won't be.
There are no significant others for my children and I wept about that this past spring. I am sort of okay with that now. I fear they will be alone in their old age, but then perhaps all of us will be even if we have children.

Inflammation; Aspirin is suppose to help .

A couple of weeks ago my husband is all excited and brings home hemp oil. They are selling it?
I finally looked it up. I know every body says it helps on seizures, but I am not messing with hemp. Well I see that it is not the mind altering stuff, nothing like that at all. It does not contain the THC. It is legal. It fights inflammation. Well, I am so slow on things. So I am just slow Visitor.

Probably Canadensis albicans is in my brain. I think it is in my ear?
We are a mess I think.

There will be no apology or acknowledgment of what has been done to us. Just a quiet changing of things after Del Bigtree, Mark Blaxill, and JF Kennedy Jr, gets done with a bunch of deep state health officials.

I got to go pour some more water over my jars of sauerkraut and then to bed for sweet dreams are Thank you Visitor:








There are no grand children and there won't be.

Inflammation; Aspirin is suppose to help .


We are a mess I think.


I got to go pour some more water over my jars of sauerkraut and then to bed for sweet dreams are made of these-----


Benedetta, I meant respond after your post, but got immersed in thought. I do appreciate your reply: "I will chew on these links a bit." Sweet Dreams to you...


A report that I have saved that is current enough and very good.



This one starts with ethanol relation, but the one a couple down o the right on Tuberculosis is another that was of interest for me.




It is known those with Autism have lot more Atopic Dermatitis.

MicroRNA-155-5p is a key regulator of allergic inflammation, modulating the epithelial barrier by targeting PKIα.


"Recent studies have demonstrated that microRNA-155-5p (miR-155-5p) plays an essential role in the regulation of allergen-induced inflammation and is overexpressed in the skin of patients with atopic dermatitis (AD), although the mechanism is unknown. In this study, silencing miR-155-5p attenuated the thickening of the epidermis in AD model and reduced the infiltration of inflammatory cells and the secretion of Th2 cytokines. Protein kinase inhibitor α (PKIα) was identified as a direct target of miR-155-5p and correlated negatively with miR-155-5p in our AD model. Fluorescence in situ hybridization showed that miR-155-5p-expressing cells were predominantly present in the epidermis. When epithelial cells were transfected with an miR-155-5p inhibitor, the expression of PKIα, occludin, and CLDN16 increased and that of TSLP decreased significantly, whereas the overexpression of miR-155-5p resulted in the opposite changes. The increased expression of PKIα and tight junction (TJ) proteins, with reduced TSLP and IL-33, was also detected in miR-155-5p-blocked mice, in both the initial and elicitation stages of AD. The expression of TJ proteins also decreased when cells were transfected with PKIα siRNA. TJ proteins increased and TSLP and IL-33 decreased significantly after the overexpression of PKIα. Our data provide the first evidence that miR-155-5p is critical for the allergic inflammation in a mouse model of AD by directly regulating PKIα and thus epithelial TJ expression. These findings suggest new therapeutic strategies that target miR-155-5p in patients with allergic disorders."


MiR-155 and other microRNAs downregulate drug metabolizing cytochromes P450 in inflammation.


A couple on Kawasaki's.

CYP2E1 Gene Polymorphisms Related to the Formation of Coronary Artery Lesions in Kawasaki Disease.


Regulatory T cell microRNA expression changes in children with acute Kawasaki disease.


Kawasaki disease (KD) is a type of systemic vasculitis syndrome related to immune dysfunction. Previous studies have implicated that dysfunctional regulatory T cells (Treg ) may be associated with the immune dysfunction in KD. In the absence of microRNAs (miRNAs), forkhead box protein 3 (FoxP3)(+)  Treg develop but fail to maintain immune homeostasis. This study was designed to investigate the effects of miR-155, miR-21 and miR-31 on Treg in children with KD. The proportions of CD4(+) CD25(+) FoxP3(+) Treg and the mean fluorescence intensity (MFI) of phosphorylated-signal transducer and activator of transcription (pSTAT)-5 and pSTAT-3 protein in CD4(+) CD25(+) Treg were analysed by flow cytometry. The concentration of interleukin (IL)-6 in plasma was measured by cytometric bead array. Real-time polymerase chain reaction was performed to detect the levels of microRNAs and associated factors in CD4(+) CD25(+) Treg . The proportion of Treg and the mRNA levels of the associated factors [FoxP3, glucocorticoid-induced tumour necrosis factor-receptor (GITR), cytotoxic T lymphocyte antigen (CTLA)-4)] were significantly lower in KD patients (P < 0·05). MiR-155 and miR-21 levels were significantly down-regulated and miR-31 expression was higher in KD patients (P < 0·05). Plasma interleukin (IL)-6 concentrations, pSTAT-3 protein levels and suppressors of cytokine signalling (SOCS)-1 mRNA expression were remarkably elevated in acute KD (P < 0·05), while pSTAT-5 protein levels were remarkably decreased in acute KD (P < 0·05). These findings were reversed after intravenous immunoglobulin treatment (P < 0·05). Our results demonstrate that FoxP3 mRNA levels were primarily affected by the miR-155/SOCS1 and the miR-31 signalling pathways. These results suggest that the decrease in FoxP3(+) Treg might be associated with decreased expression of miR-155, leading to aberrant SOCS1/STAT-5 signalling and overexpression of miR-31 in patients with acute KD.



Kawasaki disease (KD) is an acute febrile systemic vasculitis that disturbs coronary arteries. Patients' risks of adverse cardiovascular events and subclinical atherosclerosis have been found to significantly increase with polymorphisms of the human cytochrome P450. This current study aims to research the possible relationship between cytochrome P450, family 2, subfamily E and polypeptide 1 (CYP2E1) polymorphisms with KD.


We selected 6 tag single-nucleotide polymorphisms (SNPs) of the CYP2E1 gene for TaqMan allelic discrimination assay in 340 KD patients and performed analysis on the clinical phenotypes and coronary artery lesions (CALs). CAL associations of tag SNPs were adjusted for age and gender in the logistic regression.


The KD patients with a CC genotype of rs915906 demonstrated a greater proportion of CAL formation (P = 0.009). Furthermore, the GG genotype frequencies of rs2070676 showed a significantly greater risk for CAL formation in KD patients (P = 0.007). However, the SNPs of the CYP2E1 gene did not influence CAL formation in the participating KD patients either with or without high-dose acetylsalicylic acid. Using the expression quantitative trait locus analyses, we found that the SNPs associated with CAL formation in KD also affected CYP2E1 expression in certain cell types.


This study is the first to find that the risk of CAL formation is related to CYP2E1 gene polymorphisms in KD patients.



Thank you so much Visitor;

I will chew on these links a bit. No, I don't think you are autistic. Something more, I think.
Great love and a desire to have a much time as possible with our love ones, in our little flash of life on this planet.

Don't forget to be kind to yourself though.


Benedetta, I won't presume with certainty. But, you referred to DAO in another recent post and as I had recently mentioned this in this thread I thought you may have been prompted to see new associations with it from what I had recently posted. I had mentioned mast cells in the gut bug thread and had seen their involvement forever. I also cited them a few times early in this thread series. I though that most would see their other involvement from those posts and from my post on "brain allergies". Any way in case you are trying to understand these matters here are ac coup[le links that give clarity to matters I had seen many years before these sites were posted. I am not good at understanding at were others may understand a matter.
I may be a bit autistic myself. They say it takes one to know one. I don't think I am, I am the antithesis I think.





Once an English teacher and one of my favorite artist. His Fields of Gold is exquisite.



Susan, thank you for the greeting. I have not forgotten an interchange we had here on AoA. I won't disavow what I am like at times, but I ask you please excuse my manner at times. My apologies for my petulance.

susan welch

Visitor. Happy Thanksgiving from UK and thank you for the beautiful link.


Happy Thanksgiving AoA!



Knew this for sure by 2002, but always had to believe I was a dumbass because everyone else knew better and you could not learn anything with Google unless you had a medical degree. I loathe this elite dumbass mentality. I knew all of this years before these geniuses declared it to be the fact. The medical establishment is tantamount to a cult In many ways. Their "peer reviewed" holy ones. Barf and gag me. Their arrogance not mine. I just spoke the truth. I have mentioned in this thread for a long time. I saw its relation in 1996. Dumb and Dumber. I am through wallowing on the outside because they are dense.



Dysbiotic microbiota in autistic children and their mothers: persistence of fungal and bacterial wall-deficient L-form variants in blood

Based on our hypothesis for existing microbiota of wall-deficient variants (L-forms) in human blood, we created an innovative methodology, which allowed for the development of L-form populations from blood of all investigated people. In contrast to healthy controls, blood L-forms from autistic children and their mothers converted under appropriate conditions of cultivation into detectable opportunistic bacteria and fungi, а process demonstrated by light and transmission electron microscopy. It can be distinguished into two types of states – “eubiotic” blood microbiota in healthy individuals, and “dysbiotic” in autistic children and their mothers. Remarkably, the unifying finding for autistic children and their mothers was the presence in blood of wall-free variants from life-cycle of filamentous fungi. Increased specific IgG, IgM and IgA, together with typical mold growth were a decisive argument for proven presence of Aspergillus fumigatus in almost all of the autistic children. As it was demonstrated in our previous study, filterable L-forms can be transmitted by vertical pathway from mother to child before birth. Thus, it can be suggested that autistic children may be born already colonized with fungi, while a “silent aspergillosis” could contribute or even be a leading cause for neurodevelopmental disorders in the early childhood.


The jury is out on mir-155 weighing this against the4 last post. It may be in the Goldilocks domain.

Inhibition of miR-155 Limits Neuroinflammation and Improves Functional Recovery After Experimental Traumatic Brain Injury in Mice.


Micro-RNAs (miRs) are short, noncoding RNAs that negatively regulate gene expression at the post-transcriptional level and have been implicated in the pathophysiology of secondary damage after traumatic brain injury (TBI). Among miRs linked to inflammation, miR-155 has been implicated as a pro-inflammatory factor in a variety of organ systems. We examined the expression profile of miR-155, following experimental TBI (controlled cortical impact) in adult male C57Bl/6 mice, as well as the effects of acute or delayed administration of a miR-155 antagomir on post-traumatic neuroinflammatory responses and neurological recovery. Trauma robustly increased miR-155 expression in the injured cortex over 7 days. Similar TBI-induced miR-155 expression changes were also found in microglia/macrophages isolated from the injured cortex at 7 days post-injury. A miR-155 hairpin inhibitor (antagomir; 0.5 nmol), administered intracerebroventricularly (ICV) immediately after injury, attenuated neuroinflammatory markers at both 1 day and 7 days post-injury and reduced impairments in spatial working memory. Delayed ICV infusion of the miR-155 antagomir (0.5 nmol/day), beginning 24 h post-injury and continuing for 6 days, attenuated neuroinflammatory markers at 7 days post-injury and improved motor, but not cognitive, function through 28 days. The latter treatment limited NADPH oxidase 2 expression changes in microglia/macrophages in the injured cortex and reduced cortical lesion volume. In summary, TBI causes a robust and persistent neuroinflammatory response that is associated with increased miR-155 expression in microglia/macrophages, and miR-155 inhibition reduces post-traumatic neuroinflammatory responses and improves neurological recovery. Thus, miR-155 may be a therapeutic target for TBI-related neuroinflammation.


Traumatic brain injury; miR-155; microglial activation; neuroinflammation; neuroprotection



I often state things as though possible as in the last post concerning CYP2E1. This is mainly because we have no tests for many of the factors I speak about. The connection of treatment/symptoms and outcomes with many layers of interconnections are very clear about their involvement. Mir-155 is a double-edged sword. The involvement could develop slowly or abruptly. MIR-155 may lead to weight gain and the invoking of Leptin as well as a neuroprotectant may be a part of a good amount of Autism. I posted a link to this MIR found in the Amygdala of those with Autism not many posts back.

Induction of miR-155 after Brain Injury Promotes Type 1 Interferon and has a Neuroprotective Effect



One of the very earlier considerations in our case was the effect of Isoniazid on my wife's mother and the persistence of its effect in her system. It is possible issues with CYP2E1 were part of the reason for her susceptibility to TB and mycoplasma. It also may be that Isoniazid disturbed her liver and enzymatic function and microbiome and ultimately her immune system. This would have effected my wife when she was in the womb.If and when a vaccine given to my wife's mother could be involved I have no idea. I do think my wife, although have genetic predisposition, epigenetic effects, very early on dysbiotic gut. and MIA in her gestation already, was further effected by vaccines. The first report abstract was one I found early on and it is more clearly a part as research has elucidated its relationship.

Isoniazid interactions.


Isoniazid is an antituberculous drug that is usually administered for nine to 12 months. The potential for clinically important interactions exists because this drug is a potent inhibitor of drug metabolism. Studies and case reports have shown that isoniazid inhibits the metabolism of several drugs, including phenytoin, carbamazepine, anticoagulants, benzodiazepines, and vitamin D. Furthermore, isoniazid inhibits both monoamine oxidase and diamine oxidase (histaminase). Additional study is required to document the clinical significance of other isoniazid interactions. Future investigations will identify new isoniazid interactions.


Placental DNA methylation levels at CYP2E1 and IRS2 are associated with child outcome in a prospective autism study.


DNA methylation acts at the interface of genetic and environmental factors relevant for autism spectrum disorder (ASD). Placenta, normally discarded at birth, is a potentially rich source of DNA methylation patterns predictive of ASD in the child. Here, we performed whole methylome analyses of placentas from a prospective study MARBLES (Markers of Autism Risk in Babies-Learning Early Signs) of high-risk pregnancies. A total of 400 differentially methylated regions (DMRs) discriminated placentas stored from children later diagnosed with ASD compared to typically developing controls. These ASD DMRs were significantly enriched at promoters, mapped to 596 genes functionally enriched in neuronal development, and overlapped genetic ASD risk. ASD DMRs at CYP2E1 and IRS2 reached genome-wide significance, replicated by pyrosequencing and correlated with expression differences in brain. Methylation at CYP2E1 associated with both ASD diagnosis and genotype within the DMR. In contrast, methylation at IRS2 was unaffected by within DMR genotype but modified by preconceptional maternal prenatal vitamin use. This study therefore identified two potentially useful early epigenetic markers for ASD in placenta.


The landscape of copy number variations in Finnish families with autism spectrum disorders.


Rare de novo and inherited copy number variations (CNVs) have been implicated in autism spectrum disorder (ASD) risk. However, the genetic underpinnings of ASD remain unknown in more than 80% of cases. Therefore, identification of novel candidate genes and corroboration of known candidate genes may broaden the horizons of determining genetic risk alleles, and subsequent development of diagnostic testing. Here, using genotyping arrays, we characterized the genetic architecture of rare CNVs (<1% frequency) in a Finnish case-control dataset. Unsurprisingly, ASD cases harbored a significant excess of rare, large (>1 Mb) CNVs and rare, exonic CNVs. The exonic rare de novo CNV rate (∼22.5%) seemed higher compared to previous reports. We identified several CNVs in well-known ASD regions including GSTM1-5, DISC1, FHIT, RBFOX1, CHRNA7, 15q11.2, 15q13.2-q13.3, 17q12, and 22q11.21. Additionally, several novel candidate genes (BDKRB1, BDKRB2, AP2M1, SPTA1, PTH1R, CYP2E1, PLCD3, F2RL1, UQCRC2, LILRB3, RPS9, and COL11A2) were identified through gene prioritization. The majority of these genes belong to neuroactive ligand-receptor interaction pathways, and calcium signaling pathways, thus suggesting that a subset of these novel candidate genes may contribute to ASD risk. Furthermore, several metabolic pathways like caffeine metabolism, drug metabolism, retinol metabolism, and calcium-signaling pathway were found to be affected by the rare exonic ASD CNVs. Additionally, biological processes such as bradykinin receptor activity, endoderm formation and development, and oxidoreductase activity were enriched among the rare exonic ASD CNVs. Overall, our findings may add data about new genes and pathways that contribute to the genetic architecture of ASD.


In the search for reliable biomarkers for the early diagnosis of autism spectrum disorder: the role of vitamin D.

El-Ansary A1,2,3,4, Cannell JJ5, Bjørklund G6, Bhat RS7, Al Dbass AM7, Alfawaz HA8, Chirumbolo S9, Al-Ayadhi L3,4,10.


Autism spectrum disorder (ASD) affects about 1% of the world's population. Vitamin D is thought to be essential for normal brain development and modulation of the immune system. Worldwide about 1 billion people are affected by vitamin D deficiency. High-sensitivity C-reactive protein (hs-CRP), cytochrome P450 2E1 (CYP2E1) and 8-hydroxy-2'-deoxyguanosine (8-OH-dG) are biomarkers related to inflammation and oxidative stress. In the present study, these biomarkers were together with serum 25-hydroxyvitamin D (25(OH)D3) analyzed in 28 (mean age seven years) Saudi male patients with ASD. The study was conducted to determine if there is any relationship between vitamin D levels, the tested biomarkers and the presence and severity of ASD. The hope was to identify if these biomarkers may be useful for early ASD diagnosis. The Childhood Autism Rating Scale (CARS) and the Social Responsiveness Scale (SRS) were used to measure autism severity. The results of the ASD children were compared with 27 age and gender-matched neurotypical controls. The data indicated that Saudi patients with ASD have significantly lower plasma levels of 25(OH)D3 than neurotypical controls (38 ng/ml compared to 56 ng/ml, respectively; [P = 0.001]). Surprisingly, the levels of CYP2E1 were lower in the children with ASD than the neurotypical controls (0.48 ± 0.08 vs. 69 ± 0.07 ng/ml, respectively; P = 0.001). The ASD children also had significantly higher levels of hs-CRP (0.79 ± 0.09 vs. 0.59 ± 0.09 ng/ml, respectively; P = 0.001) and 8-OH-dG (8.17 ± 1.04 vs. 4.13 ± 1.01 ng/ml, respectively; P = 0.001, compared to neurotypical age and gender-matched controls. The values for hs-CRP and 8-OH-dG did not correlate [P < 0.001] with autism severity. There was found a relationship between autism severity on the CARS scale and the levels of 25(OH)D3 and CYP1B1. But this was not found for SRS. All four biomarkers seemed to have good sensitivity and specificity, but the sample size of the present study was too small to determine clinical usefulness. The findings also indicate that inadequate levels of vitamin D play a role in the etiology and severity of autism. Furthermore, the results of the present study suggest the possibility of using 25(OH)D3, CYP1B1, hs-CRP and 8-OH-dG, preferably in combination, as biomarkers for the early diagnosis of ASD. However, further research is needed to evaluate this hypothesis.


Relationship of anti-tuberculosis drug-induced liver injury and genetic polymorphisms in CYP2E1 and GST.



Treatment of tuberculosis (TB) can result in Drug-Induced Liver Injury (DILI) since hepatotoxic metabolites are formed during the biotransformation of isoniazid (INH). DILI can be related to the genetic profile of the patient. Single nucleotide polymorphisms in the CYP2E1 gene and GSTM1 and GSTT1 deletion polymorphisms have been associated with adverse events caused by INH.


To characterize the genetic polymorphisms of CYP2E1, GSTT1 and GSTM1 in TB carriers.


This is an observational prospective cohort study of 45 patients undergoing treatment of TB. PCR-RFLP and multiplex-PCR were used.


The distribution of genotypic frequency in the promoter region (CYP2E1 gene) was: 98% wild genotype and 2% heterozygous. Intronic region: 78% wild genotype; 20% heterozygous and 2% homozygous variant. GST enzyme genes: 24% Null GSTM1 and 22% Null GSTT1. Patients with any variant allele of the CYP2E1 gene were grouped in the statistical analyses.


Patients with the CYP2E1 variant genotype or Null GSTT1 showed higher risk of presenting DILI (p=0.09; OR: 4.57; 95% CI: 0.75-27.6). Individuals with both genotypes had no increased risk compared to individuals with one genotype.


Mitochondrial CYP2E1 is sufficient to mediate oxidative stress and cytotoxicity induced by ethanol and acetaminophen.


Several cytochromes P450 (CYPs) are not only located in the endoplasmic reticulum but also within mitochondria. One such CYP is CYP2E1 which metabolizes numerous substrates and generates significant amount of reactive oxygen species. The presence of CYP2E1 in these organelles raises questions regarding its physiological role but also its possible deleterious effects in the context of drug-induced cytotoxicity. The aim of our study was to investigate the role of mitochondrial CYP2E1 in the toxicity of acetaminophen and ethanol. Hence the effects of these two compounds in cells expressing CYP2E1 in mitochondria only, or in both endoplasmic reticulum and mitochondria, were compared to those observed in mock-transfected cells. Our results indicated that when acetaminophen or ethanol were used as CYP2E1 substrates, the exclusive localization of CYP2E1 within mitochondria was sufficient to induce reactive oxygen species overproduction, depletion of reduced glutathione, increased expression of mitochondrial Hsp70, mitochondrial dysfunction and cytotoxicity. Importantly, these harmful events happened despite lower cellular level and activity of CYP2E1 when compared to cells expressing CYP2E1 in both endoplasmic reticulum and mitochondria, and this was particularly obvious with acetaminophen. Taken together, these data suggest that mitochondrial CYP2E1 could play a major role in drug-induced oxidative stress and cell demise.


Maternal Gestational Diabetes Mellitus and Newborn DNA Methylation: Findings From the Pregnancy and Childhood Epigenetics Consortium.



Maternal gestational diabetes mellitus (GDM) has been associated with adverse outcomes in the offspring. Growing evidence suggests that the epigenome may play a role, but most previous studies have been small and adjusted for few covariates. The current study meta-analyzed the association between maternal GDM and cord blood DNA methylation in the Pregnancy and Childhood Epigenetics (PACE) consortium.


Seven pregnancy cohorts (3,677 mother-newborn pairs [317 with GDM]) contributed results from epigenome-wide association studies, using DNA methylation data acquired by the Infinium HumanMethylation450 BeadChip array. Associations between GDM and DNA methylation were examined using robust linear regression, with adjustment for potential confounders. Fixed-effects meta-analyses were performed using METAL. Differentially methylated regions (DMRs) were identified by taking the intersection of results obtained using two regional approaches: comb-p and DMRcate.


Two DMRs were identified by both comb-p and DMRcate. Both regions were hypomethylated in newborns exposed to GDM in utero compared with control subjects. One DMR (chr 1: 248100345-248100614) was located in the OR2L13 promoter, and the other (chr 10: 135341870-135342620) was located in the gene body of CYP2E1. Individual CpG analyses did not reveal any differentially methylated loci based on a false discovery rate-adjusted P value threshold of 0.05.


Maternal GDM was associated with lower cord blood methylation levels within two regions, including the promoter of OR2L13, a gene associated with autism spectrum disorder, and the gene body of CYP2E1, which is upregulated in type 1 and type 2 diabetes. Future studies are needed to understand whether these associations are causal and possible health consequences.


Tylenol may be involved or a trigger in some cases, or a synergy with a vaccine at times.

The role of oxidative stress, inflammation and acetaminophen exposure from birth to early childhood in the induction of autism.

Author information


The wide range of factors associated with the induction of autism is invariably linked with either inflammation or oxidative stress, and sometimes both. The use of acetaminophen in babies and young children may be much more strongly associated with autism than its use during pregnancy, perhaps because of well-known deficiencies in the metabolic breakdown of pharmaceuticals during early development. Thus, one explanation for the increased prevalence of autism is that increased exposure to acetaminophen, exacerbated by inflammation and oxidative stress, is neurotoxic in babies and small children. This view mandates extreme urgency in probing the long-term effects of acetaminophen use in babies and the possibility that many cases of infantile autism may actually be induced by acetaminophen exposure shortly after birth.


Can autism be triggered by acetaminophen activation of the endocannabinoid system?


Acetaminophen use in children has been associated with increased autism risk. Recent evidence suggests that acetaminophen's analgesic actions result from activation of the endocannabinoid system, and activation of this system can have neuromodulatory consequences during development. This investigation was performed to determine if there is evidence to support the hypothesis that acetaminophen use can trigger autism by activation of the endocannabinoid system.



I had tried to post this before the last post as they both speak to collagen and T-Cells and show relation. Maybe I was posting too much of the article.

Surplus of immune cells may mark brains of autistic people

"Blood vessels in the brains of more than half of autistic people have an unusually large number of immune cells called T cells, according to an analysis of postmortem tissue1. This excess may damage cells that form a protective lining for the brain.

The findings jibe with results showing elevated levels of immune molecules, as well as hyperactive immune cells called microglia, in the brains of people with autism2.

“There’s just a chronic inflammatory state,” says the new study’s lead investigator, Matthew Anderson, chief of neuropathology at Beth Israel Deaconess Medical Center in Boston, Massachusetts.

The team found that blood vessels with excess T cells tend to be surrounded by debris from cells that help form part of the blood-brain barrier.

“That’s novel and provocative, and I think it is something that has to be verified and replicated,” says S. Hossein Fatemi, professor of psychiatry at the University of Minnesota, who was not involved in the study. “This is purely a descriptive study.”

Anderson’s team stumbled upon their findings during routine microscopic examinations of tissue from Autism BrainNet, a repository of brain tissue from people with autism. (Anderson is lead neuropathologist for the repository.)

Peering under a microscope, Anderson says, he noticed that samples from autistic people tend to contain numerous round ‘blebs’ — tiny droplets of debris released from cells. These blebs littered the spaces that separate blood vessels from brain tissue.

“I kept seeing little foci of those,” Anderson says. “I’ve never seen that before in any other condition.”

His team then systematically looked for the blebs in samples from 25 people with autism and 30 controls who ranged in age from 1 to 68 years. They first focused on blood vessels and the spaces around them in tissue from the cerebral cortex, the brain’s outer layer.

They suspected, and were able to confirm, that the blebs had been released from nearby astrocytes. These cells surround blood vessels and form part of the blood-brain barrier.

The brains of autistic people have much larger swaths containing blebs than controls do, the team found. The findings appeared 8 October in Annals of Neurology.

Under attack:

Cells often release blebs when attacked by a subset of immune cells called cytotoxic T cells. And the team found that these T cells do often cluster in blood vessels near the blebs.

About 65 percent of the autistic people have more T cells in the cerebral cortex than controls do; they also show excess T cells in seven of eight other brain regions the team examined.

The more T cells a person had, the more astrocyte debris. The space surrounding blood vessels also tends to be enlarged in people with autism, and contains excess collagen, a protein produced in response to tissue damage.

The findings hint that T cells seek out and destroy the astrocytes, Anderson says.

Still, it is unclear why these T cells accumulate in the autism brain or why they might attack this lining. The cells are usually responsible for fighting off viruses and are implicated in autoimmune conditions.

The T cells may be innocent bystanders, attracted to the scene by molecules released after astrocytes are damaged by some other cause.

“Are they damaging those cells, or are they responding to the damage of those cells?” says Judy Van de Water, professor of internal medicine at the University of California, Davis, who was not involved in the study. “You cannot, from this type of study, answer that question.”

Anderson and his team are trying to identify tags on astrocytes that might attract the T cells. They are also exploring whether the damage to the barrier occurs in utero."



hmmm...familiar actors

Angiotensin receptor blockers suppress antigen-specific T cell responses and ameliorate collagen-induced arthritis in mice.


The renin-angiotensin system plays an important role in the regulation of cardiovascular, renal, and endocrine functions. Recent studies have demonstrated that angiotensin II has proinflammatory effects that may contribute to the pathogenesis of immune-mediated diseases. We used the collagen-induced arthritis (CIA) model to investigate the influence of angiotensin II receptor blockers (ARBs) on antigen-specific immune responses and determine whether ARBs have preventive or therapeutic effects on the development of arthritis.


We administered ARBs (olmesartan, candesartan, and telmisartan) to mice and evaluated antigen-specific T cell proliferation and cytokine production following immunization with ovalbumin (OVA) or type II collagen in Freund's complete adjuvant (CFA) or aluminum hydroxide (alum). Next, we induced CIA in DBA/1 mice and administered olmesartan. The severity and incidence of arthritis were scored according to clinical manifestations, and joint tissue sections were examined histopathologically.


ARBs severely suppressed lymphocyte proliferation and interferon-gamma production in mice immunized with OVA or type II collagen in CFA. Olmesartan also suppressed lymphocyte proliferation in mice immunized with ovalbumin in alum. In the CIA model, olmesartan reduced the mean arthritis score and the incidence of severe arthritis, even when it was administered only after disease onset. Histopathologic findings for joint destruction were improved in olmesartan-treated mice.


ARBs suppressed antigen-specific immune responses for Th1 and Th2 in vivo. Furthermore, olmesartan suppressed the development of severe arthritis and joint destruction in the CIA model. These findings suggest that ARBs may have therapeutic potential in rheumatoid arthritis.



For clarity, I am not suggesting ADNP mutations are the cause of most autism. I am saying that effects bearing on this gene and many others can be part of Vasoactive Intestinal Peptide effects, or lack thereof. In common autism and syndromes in addition to related Alzheimer brain disease. Involved in much Autism ass put forth in the below: {I am not negating vaccine effects in triggering the cascade in an undetermined amount of cases. I generally believe the parents/caregivers.

Impaired neurodevelopmental pathways in autism spectrum disorder: a review of signaling mechanisms and crosstalk



In the Gene Card entry for ADNP referred to in the last post you will see its relationship with Vasoactive Intestinal Peptide. Here is a quote for the ADNP entry.

Entrez Gene Summary for ADNP Gene

"Vasoactive intestinal peptide is a neuroprotective factor that has a stimulatory effect on the growth of some tumor cells and an inhibitory effect on others. This gene encodes a protein that is upregulated by vasoactive intestinal peptide and may be involved in its stimulatory effect on certain tumor cells. The encoded protein contains one homeobox and nine zinc finger domains, suggesting that it functions as a transcription factor. This gene is also upregulated in normal proliferative tissues. Finally, the encoded protein may increase the viability of certain cell types through modulation of p53 activity. Alternatively spliced transcript variants encoding the same protein have been described. [provided by RefSeq, Jul 2008]"

The autism-mutated ADNP plays a key role in stress response.




Vasoactive intestinal peptide (VIP) regulates activity-dependent neuroprotective protein (ADNP) expression in vivo.


"Vasoactive intestinal peptide (VIP) is an important mediator of development during the neural tube closure period of embryogenesis and may regulate, in part, the expression of activity-dependent neuroprotective protein (ADNP), which is essential for neural tube closure and embryogenesis. To evaluate the impact of VIP expression in vivo on ADNP and the related protein ADNP2 the current study examined gene expression in adult wild-type (VIP +/+) and VIP null (VIP -/-) offspring of VIP deficient mothers (VIP+/-) comparing them to wild-type offspring of wild-type mothers. Quantitative real time polymerase chain reaction (PCR), using an ABI Prisma cycler revealed regionally specific reductions of ADNP mRNA in the brains of VIP null mice compared with the brains of wild-type offspring of a wild-type mother. ADNP was significantly reduced in the cortex and hypothalamus of VIP null mice, but not in the hippocampus or thalamus. ADNP2 exhibited a similar pattern but reached a statistically significant reduction only in the hypothalamus. The mRNA for ADNP and ADNP2 also tended to be reduced in the cortex and hippocampus of the wild-type littermates of the VIP null mice, indicating that the VIP genotype of the mother may have had an impact on the ADNP expression of her offspring, regardless of their own VIP genotype. These results showed that VIP regulated brain ADNP expression in a regionally specific manner and indicated that both maternal and offspring VIP genotype may influence ADNP expression in the brain."


Nitric oxide-NGF mediated PPTA/SP, ADNP, and VIP expression in the peripheral nervous system.


Helpful to read.
Vasoactive intestinal peptide


On another front, but ultimately part of the picture in light of MTHFR and autism ties and for other system connections.

The role of the MTHFR gene in migraine.


"Migraine is a common neurological disorder and is characterized by debilitating head pain and an assortment of additional symptoms which can include nausea, emesis, photophobia, phonophobia, and occasionally, visual sensory disturbances. A number of genes have been implicated in the pathogenesis of this disease, including genes involved in regulating the vascular system. Of particular importance are the methylenetetrahydrofolate reductase (MTHFR) gene and the role it plays in migraine with aura. Migraine with aura has previously been shown to have a significant comorbidity with stroke, making the vascular class of genes a priority for migraine studies. In this report, we outline the importance of the MTHFR gene in migraine and also discuss the use of a genetic isolate to investigate MTHFR genetic variants. From this study, 3 MTHFR single nucleotide polymorphisms showing association with migraine in the Norfolk Island population have been identified, thus reinforcing the potential role of MTHFR in migraine susceptibility. Further studies will continue to build a gene profile of variants involved in the complex disease migraine and improve understanding of the underlying genetic causes of this disorder."


Heard Magnesium Sulfate for some Autism?

Intravenous magnesium sulfate rapidly alleviates headaches of various types.


Can't read the report, but the tile relates to the way this would cause a person to deal with toxins/detox and carcinogenic effect. and likely hyperemesis gravidarum.

Emerging Role of Polymorphisms of the MTHFR Gene in Systemic Carcinogenesis Besides Their Role in Migraines



There is so much interconnection. Here is just a little.
Mentioned OPRD1 and Psychopathy a few posts back. Here is a list of miRNA Targets Report for gene MIR155.

Top of the list is CCND1 followed by AGTR1{Angiotensin II Receptor Type 1} includes OPRM1 and OPRL1 and many others listed in this thread and the "Gut Bug" thread that are all part of the machinery of dysfunction..

miRNA Targets Report for gene MIR155

CCND1 Gene


Discovery of autism/intellectual disability somatic mutations in Alzheimer's brains: mutated ADNP cytoskeletal impairments and repair as a case study.





I am drifting in far galaxies and anyone is free to considers these facts. I have seen these links for years, but did not like their implications.









A link will not suffice. The study worth reading too. This had to be the case.

Immune system lends the brain a hand

"Researchers have discovered that the immune system helps out the brain, in the absence of any disease, by making a chemical messenger that boosts memory.

The study was in mice, but senior author Bruno Silva-Santos, from the University of Lisbon, Portugal, says the finding could lead to dietary recommendations to improve memory in people.

The study is part of a rising tide of research upending the traditional view that the immune system exists only to fight infection and tumours.

The authors point out that disease is relatively rare, and so maintaining a complex system of immunity would impose a big cost if busting microbes and cancer were the only benefit.

Already, they say, immunity is known to have non-disease roles in temperature control and bone repair. But to accept that the immune system could be a major player in the everyday workings of the brain, another shibboleth in medicine must fall by the wayside.

“The brain was seen as an immune privileged organ, meaning that it would be completely shielded by the blood brain barrier and completely hermetic to the peripheral immune system,” explains senior author Julie Ribot, in a linked video.

Recently, says Ribot, it has been found that lymphatic vessels, which transport infection-fighting white blood cells, are present in the lining of the brain, called the meninges.

“This is really important,” says Ribot, “because it suggests that actually the brain and the immune system do constantly communicate, even when we are not sick.”

The presence of a workaday brain-immune relationship is born out in recent studies showing white cells, called T lymphocytes, are key for spatial learning and social behaviour.

But the team had a hunch there was an even broader connection.

They believed a type of lymphocyte known as a gamma delta T cell, which is resident in the meninges, could be crucial for memory. So they devised some clever experiments in mice that were specifically engineered to lack gamma delta cells.

When they put those mice to the test in a maze, the critters’ short-term memory – the bit that helps you remember what you had for lunch today, but not last week – was shot.

The finding was pleasingly consistent with the researchers’ theory, but how those gamma delta cells were helping memory came as a curve ball.

“We thought gamma delta cells would be pro-cognitive,” says Silva-Santos.

“What was very surprising was that … the molecule they secrete to endow cognition is actually IL-17,” he says.

Surprising, explains Silva-Santos, because IL-17 (interleukin-17) is what’s known as a “pro-inflammatory cytokine”. It’s something of a bad boy, known to cause inflammation and contribute to disease, notably multiple sclerosis.

But IL-17, the researchers found, is also a trigger for brain derived neurotrophic factor, (BDNF) a prolific neuron fertiliser that enhances signalling between brain cells in the hippocampus, a major memory centre.

The team now thinks IL-17 has to be kept in the Goldilocks zone – too much and you get inflammation and disease, too little and memory suffers.

Silva-Santos has some ideas on how we might one day get IL-17 just right.

“What will be important to know is what are the factors that regulate these basal levels of IL-17... so that we can, for instance through diet, because we have realised that vitamins can regulate this process ... have enough IL-17 in our brains, in our meninges, to guarantee proper short term learning,” he says.


link to study
Meningeal γδ T cell–derived IL-17 controls synaptic plasticity and short-term memory



James Taylor - Something In The Way She Moves



Not a surprise. Very glad this was studied.

Increased Expression of miR-155p5 in Amygdala of Children With Autism Spectrum Disorder.


"MiR-155p5 is a pro-inflammatory microRNA reported to be involved in several neurol-inflammatory diseases. Autism spectrum disorder (ASD) is a neurodevelopmental condition characterized by impaired social interactions and communication, as well as stereotypic movements. Inflammation of the brain due to activation of microglia has been reported in ASD. We investigated miR-155p5 gene expression in postmortem human brain tissues [amygdala and dorsolateral prefrontal cortex regions (DLPFC)]. There was significant increase of miR-155p5 in amygdala (P ≤ 0.0001), but not in DLFC, in ASD children (n = 8) compared to non-ASD (n = 7) controls. The increased gene expression of miR-155p5 in amygdala of children of ASD support the presence of localized inflammation in the brain and indicates miR-155p5 may be targeted for therapy of ASD. Autism Res 2019. © 2019 International Society for Autism Research, Wiley Periodicals, Inc. LAY SUMMARY: The pathogenesis of autism spectrum disorder (ASD) is still unknown. Our data of increased gene expression of miR-155p5 in brains of children with ASD support the presence of localized inflammation in the amygdala and indicates that miR-155p5 may be targeted for therapy of ASD and other neurodegenerative diseases."



Abnormal expression of genes in psychopathy

"The expression of many genes that have previously been associated with autism is abnormal also in violent psychopathy, a new study shows..."

"The study shows that psychopathy is associated with robust alterations in the expression of genes and immune-response-related molecular pathways. Several of these genes have also been linked to autism. In neurons, psychopathy was associated with marked upregulation of RPL10P9 and ZNF132, and downregulation of CDH5 and OPRD1. In astrocytes, RPL10P9 and MT-RNR2 were upregulated. The expression of these genes explained 30-92% of the variance of psychopathic symptoms. Psychopathy was also associated with altered expression of proteins related to glucose metabolism and the opioid system."

"Several earlier studies have suggested that violent and psychotic behaviour are associated with alterations in glucose metabolism and opioidergic neurotransmission. The new findings support the idea of abnormal opioid system function being a factor underlying psychopathy. This suggests that using long-lasting injections of naltrexone or buprenorphine to balance the opioid system could be a feasible treatment for psychopathy."


As you may know Low Dose Naltrexone Therapy has been discussed and tried for years on some with Autism.

This has some bearing in our case, and I think ALZ and ASD share something in regard to mir-155.



"Neuroinflammation has important effects on cognitive functions in the pathophysiological process of Alzheimer's Disease (AD). In the current report, we determined the effects of microRNA-155 (miR-155) on the levels of IL-1β, IL-6 and TNF-α, and their respective receptors in the hippocampus using a rat model of AD.


Real-time RT-PCR, ELISA and western blot analysis were used to examine the miR-155, PICs and PIC receptors. The Morris water maze and spatial working memory tests were used to assess cognitive functions.


miR-155 was increased in the hippocampus of AD rats, accompanied by amplification of IL-1β, IL-6 and TNF-α. Intracerebroventricular infusion of miR-155 inhibitor, but not its scramble attenuated the increases of IL-1β, IL-6 and TNF-α and upregulation of their receptors. MiR-155 inhibitor also attenuated upregulation of apoptotic Caspase-3 in the hippocampus of AD rats. Notably, inhibition of miR- 155 or PIC receptors largely recovered the impaired learning performance in AD rat.


We showed the critical role of miR-155 in regulating the memory impairment in AD rats likely via engagement of neuroinflammatory mechanisms, suggesting that miR-155 and its signaling molecules may present prospects in preventing and/or improving the development of the impaired cognitive functions in AD."




Truly excellent summarizing piece here. Includes some good things on vaccination.

Innate Immunity and Neuroinflammation in Neuropsychiatric Conditions Including Autism Spectrum Disorders: Role of Innate Immune Memory



Tchaikovsky: Suite for Orchestra No.4 in G Major, Op.61, TH.34 - "Mozartiana" - 3. Preghiera Prayer



In retrospect some pieces summarize well aspect5s of the biological pathologies. I find this piece to be one. I am posting the abstract, the link to the whole is at the bottom.

Is Encephalopathy a Mechanism to Renew Sulfate in Autism?

Stephanie Seneff 1,*, Ann Lauritzen 2, Robert M. Davidson 3 and Laurie Lentz-Marino 4

Abstract: This paper makes two claims: (1) autism can be characterized as a chronic low-grade encephalopathy, associated with excess exposure to nitric oxide, ammonia and glutamate in the central nervous system, which leads to hippocampal pathologies and resulting cognitive impairment, and (2), encephalitis is provoked by a systemic deficiency in sulfate, but associated seizures and fever support sulfate restoration. We argue that impaired synthesis of cholesterol sulfate in the skin and red blood cells, catalyzed by sunlight and nitric oxide synthase enzymes, creates a state of colloidal instability in the blood manifested as a low zeta potential and increased interfacial stress. Encephalitis, while life-threatening, can result in partial renewal of sulfate supply, promoting neuronal survival. Research is cited showing how taurine may not only help protect neurons from hypochlorite exposure, but also provide a source for sulfate renewal. Several environmental factors can synergistically promote the encephalopathy of autism, including the herbicide, glyphosate, aluminum, mercury, lead, nutritional deficiencies in thiamine and zinc, and yeast overgrowth due to excess dietary sugar. Given these facts, dietary and lifestyle changes, including increased sulfur ingestion, organic whole foods, increased sun exposure, and avoidance of toxins such as aluminum, mercury, and lead, may help to alleviate symptoms or, in some instances, to prevent autism altogether.

Keywords: encephalitis; autism; nitric oxide; cholesterol sulfate; ammonia; aluminum; mercury; lead; glyphosate; seizures; taurine



Kind of think anyone reading my posts thinks I have lost my marbles. Very well may be the case and I have no clue where they went. I doubt thimerosal is the only activators of Hyaluronic Acid as autoimmunity and other immune cells{possibly mast cells} could elicit endothelial Hyaluronic Acid.

Posted this in 2012 in this thread.

Cytoprotective effect of hyaluronic acid and hydroxypropyl methylcellulose against DNA damage induced by thimerosal in Chang conjunctival cells.



Thimerosal triggers hyaluronic acid it may protect the eyes and other tissue at the expense of possibly detrimental microglial activation, though the gut microbiome may connect to this as well or in addition.

This was just released.

Neuroscientists Identify Surprising Brain Action of Cartilage Component, Hyaluronic Acid

"In a study published in the journal Brain, Behavior and Immunity, Ning Quan, Ph.D., lead author, a professor of biomedical science in FAU's Schmidt College of Medicine and a member of I-BRAIN, and collaborators, have discovered that hyaluronic acid may be the key in how an immune signal moves from the blood stream to the brain, activating the brain's resident immune cells, the microglia.

This unsuspected molecule may be the main signal passed between these cells, and this new discovery could lead to novel opportunities to shut down brain inflammatory responses. Findings from this study have important implications for better treatments for stroke, neurodegenerative diseases, as well as head injuries.

"We normally think of hyaluronic acid with respect to cartilage formation and also for its role in many processes including cancer progression and metastasis," said Quan. "However, what we have uncovered in our study is a completely unique role for this molecule. We have been able to document a connection between the blood cells and the brain cells, showing that the activating signal passed between these cells is hyaluronic acid."

Quan and collaborators from the Sichuan University, The Ohio State University, and the University of Illinois Urbana-Champaign, demonstrate that inflammation in the central nervous system is oftentimes quenched or restricted, as neurons are extremely vulnerable to inflammation-caused damages. However, this inflammation can be aberrantly amplified through endothelial cell-microglia crosstalk when the brain constantly receives inflammatory signals. Quan's work identified hyaluronic acid as the key signal released by endothelial cells to stimulate microglia and promote oxidative damage.

"To prevent the inflammation from being intensified in the brain, you have to stop the communication between the two cell types," said Xiaoyu Liu, Ph.D., another corresponding author of the study in FAU's Schmidt College of Medicine and I-BRAIN. "We found ascorbyl palmitate, also known as 'Vitamin C Ester,' to be quite effective in inhibiting microglia and reducing the production of inflammatory hyaluronic acid."



Life is but a dream, and I have not yet learned how to communicate in this incredible world that has revealed itself. I have given it my all but I cannot bring together all that you folks are communicating and though sir out the world. It is very difficult to exist I'll sing but not truly understanding. May God have mercy on my soul.


I can't end with a lie. I stated in the last post that her condition was a complex biological and spiritual condition. It was not spiritual in any degree. A subliminal desire to make it fit into some construct made me say that. Whatever spiritual is she has now, she did not before and this is no small matter. God's country is internal, not geographic for me. Geographic tongue is thought to be a form of psoriasis. , one minor tidbit.



I have massive amounts of inter related knowledge gathered to shed light on all of these matters, but my way has prove to be lost on others. It is inscrutably frustrating to the point I I will cease from further attempts to elucidate these matters. Hypogammaglobulinemia is a factor, but, one I understood 23 years ago. I underestimate how poorly people make connections. In 1995 my wife had what I now think is Eosinophilic Esophagitis and had a serious condition with a esophageal diverticulum which would have required a major surgery art the time. the diverticulum retraced after six weeks of diet restriction and antibiotics. these little cues were part of deciphering what I have found the be a immensely complex biological and spiritual complex condition that gave evidence in 1996 to a fantastical reality. I don't really fault others , but I have found it rather useless to communicate these matters to others, they can eventually deduce why. My story and countless others relate, but it is too difficult for most to see it.

Here is my synoptic beginning account. Goodbye.

The collection of articles that follows the three pages of this foreword was compiled between 6/96 and 4/97. It is directed at explaining Ramona's mental condition that was a result of complex, lifelong, and to some degree progressive, biological disorders. These articles are interrelated from the perspective of its compiler as it describes her condition. Although she had no arthritis two articles about it are included as they comment on Candida.
A list of physical and mental markers that she exhibited while in this condition was as follows: 1. Almost complete inability to smell. 2. Eyes that almost constantly stayed dilated. 3. Inability to add simple math in her head. 4. Chronic gastritis, likely caused by helicobacter pylori, producing hypochlorhydria which in turn accommodates GI bacterial overgrowth constituting a cycle. 5. Extremely poor ability to remember dreams. 6. Frequent nausea & vomiting along with frequent carsickness. 7. Fungus ridden toenails, severe and chronic vaginal Candida infections along with recurrent urinary tract infections, and vaginal discharges apparently from clostridia and various other microorganisms. 8. Attention deficit and memory problems {often I would stand beside her and say her name 4 or 5 times before she "realized" I was speaking to her}. 9. Allergy/intolerance to sulfa drugs. 10. Chronic staring into space for long periods of time or trancing while performing various tasks and getting hung up on small details for hours without realizing it. 11. Lack of self, only reacting to others in a patterned way, she had no motives or feelings of her own and was often just operating at the prompting of others. 12. Geographic tongue 13. Overtly sick half of the time. {Actually sick all of the time} 14. Avoidance of eye contact especially during serious conversation {this trait was something I noticed from the time we were married and probably not noticed by others in that it occurred in relation to my trying to get her to make decisions or give opinions concerning matters that revolved around self; i.e. why do you like or dislike this, that, or someone and why did you do this or that. 15. Occasionally I received unprovoked insults and occasionally she struck me and frequently directed unmerited aggression and belligerence towards the children and myself. She usually did not recall this behavior. 16. Chronic lack of emotional reciprocity. 17. Chronic and problematic constipation 95% of the time - diarrhea the other 5%. 18. Menstrual cycles that were never timely and severe pms. 19. Hyper-somnia. {Possibly CFIDS related virus and/or a melatonin-monoamine oxidase connection}. 20. Frequently had mucous and blood in her stool. 21. Pallor-china doll complexion. 21. Bouts of bronchitis. 22. Often talked in her sleep and usually drooled while sleeping {at times I would respond to what she said and she would carry on a short, disjointed, conversation with me as she slept}. 23. Bruised easily and developed spider veins at an early age. She normally did not know what caused her bruises.24. High pain threshold. 25. Swings of depression and euphoria related to social interaction. 26. Adopted an attitude that I was going to abandon her. 27. She shutdown when presented with our first child for nursing as she did not know how to bond or relate to him. 28. Frequently feeling her face. 29. Clumsy and accident-prone and had four minor and one major traffic accident in five years. She once ran into the back of a truck while we were going down the interstate. She was the apparent cause of a multi-car accident that totaled our car, yet she could not remember braking even though she said she knew the car in front of her was stopping. I did most of the driving until this five-year period began. During these five years she had to drive often. 30. Frequently painful intercourse. 31. Ears become very red when wrong foods are eaten. Unusual spider veins in ears. 32. Her memories were in pictures, and in second person. 33. Recurrent red facial rash with light bumps in the rash. 34. Considerable weight gain. 35. Frequent headaches and migraines often accompanied by double vision. 36. Low body temperature. 37. Sun poisoning with only brief exposure. {Possibly related to phenylic PABA in her skin interacting with sunlight.} 38. Muscle pain and frequent spasms, also joint pain. 39. Pre-pregnancy stretch marks. 40. Numerous rounds of metronidazole {Flagyl} throughout her adult life and numerous antibiotics since childhood. 41. Accelerated hair loss. 42. Eyes bulged {most notably when she was pregnant or overtly ill}. Since her examination by an allergist it has been found by blood and urine analysis that she has hypothyroidism and a low functioning adrenal gland.
Over time, with hundreds of hours of counseling and my constantly teaching her about social interaction and logical thinking, she has developed a self. But this counseling /therapy would have been useless without dealing with the maze of biological problems she had and changing her diet. The following factors gave her the ability to gain reality. She began taking Diflucan{daily} for the yeast overgrowth, taking a potent multi vitamin, taking a molybdenum supplement and liquid minerals, taking evening primrose oil, taking NAC, taking additional vitamin C, avoiding wheat & dairy & sugar and other offending foods and drugs, immuneotherapy, taking thyroid medication, and taking DHEA. For a while she took digestive enzymes, acidophilus, and black walnut extract. While on this regimen most of her problems have lessened in intensity or been eliminated except, probably, her problem with sulfa drug. Her autoimmune /metabolic phenol -sulphotransferase problem may be intractable, and only kept in check by keeping the Candida & Clostridia under control and avoiding concentrated phenols and amines.
She now can smell perfectly, her eyes dilate normally and she can add math in her head without any problem. She is still sensitive to many foods and substances and even small infractions of her diet will cause her problems. She still has much progress to make as she has had a lifetime of problems and is gaining an identity by learning a personal cognitive and social construct.
It has been posited that both Clostridia and Candida {and other yeasts}, produce phenoilic compounds. Relating to clostridia Dr. Shaw reports that the urine level of dihydroxyphenylpropionic acid decreased dramatically after Flagyl was administered to a test group of autistics. Dihydroxyphenylpropionic acid would correlate with PST deficiencies and phenolic compound involvement in some cases of autism. Dr. Shaw has found high levels of tartaric acid in the urine of autistics with yeast overgrowth and noted improvement in their symptoms after giving them Nystatin. Therefore non-phenolic compounds may be implicated as well.
I do not know if her condition was/is due to a genetic condition or began as an assault on her system in a vulnerable area by vaccinations, viruses, or bacterial infection {s}. It may be a combination of all of them. I am curious about a connection to her possibly having a C4B null gene. Other women I have discussed Ramona's condition with who also had similar physical symptoms all had experienced a serious childhood illness. In each case it was either scarletina or rheumatic fever {as a child Ramona had scarletina and a number of ear infections}. It is possible that a subset of children have a direct or latent reaction to vaccinations {possibly encephalitic} that produces vulnerability to these, and possibly other, illnesses. Elevated rubella and measles titers have been found in a number of autistic children and may indicate other disease/immune interactions. If vaccinations damage the immune system the individual would then be in a precarious immune state. Once contracting certain illnesses they may in turn trigger the onset of other immune dysfunction that causes other problems or intensify existing ones and manifest themselves in various physiological and neuropsychological ways. Antibiotics taken for these illnesses would speed the onset of this condition by destroying the proper gut ecology and setting it up for yeast overgrowth and bad bacteria colonization. I also suspect that mercury from fillings and other sources was converted to methyl mercury by yeast and bacteria in her gut. The disruption in her gut and her attendant enzymatic and metabolic problems probably relate to this as the sulfur bearing amino acids contain the necessary thiols, or sulfhydrals, to bind and remove mercury ions from the body. The methyl mercury may have in turn hindered her immune function further and may have contributed to her mental dysfunction.
Sulfa drugs contain sulfur and many contain phenols {in these cases petroleum dyes that have anti-bacterial properties}. They also inhibit the proper functioning of the majority of b-vitamins {biotin, choline, folic acid, inositol, PABA, b1, b2, b3, and b5} and inhibit the removal of certain phenolic compounds. Certain B vitamins and magnesium have been found to be therapeutic for a number of autistic individuals and they appear to be helpful, along with zinc, in some cases of schizophrenia. PST and gut problems would logically interfere with B vitamin and mineral absorption and functioning. Sulfa drugs were not the source of her problem, but they gave a dramatic presentation of the underlying metabolic/immune problem. In her case it was Bactrim DS that produced this observable reaction. This concentrated phenol - sulfur dose along with Bactrim's ability to inhibit phenolic sulfation either directly caused her symptoms by a tremendous overload of her phenol-sulphotransferase pathway and/or by stimulating her immune response due to her life long phenylic sensitivity. One sulfa tablet left her severely swollen throughout her body, her face looked like she had been beaten. The pain in her feet was so bad she could barely walk, and this lasted for a week.
When she was pregnant with Jessica her vitamin levels were nil. This was according to the doctor who admitted her to the hospital for dehydration. He put her on vitamin IV's. She was just as ill with our first child Cory. During both pregnancies she was deathly ill, lost over 20 lbs., and took phenergan {phenolic} for pastime. This helps explain why she says she remembers almost nothing of the time when she was pregnant. This phenylic sensitivity may also explain why synthetic clothing {panty hose, bras, and dresses made from nylon {made from petroleum and has phenolic compounds in it} caused severe itching with panty hose leaving her digging at her legs and reaching for the Benadryl. Benadryl would then take its toll on her, as it is actively diphenhydramine. Ramona generally had dry itchy skin about her legs. Other chemicals seem to effect her also. Rayon is probably also a culprit as the compounds ammonium hydroxide, carbon disulfide, and ethyl acetate are used in its production. The residues of these compounds in clothing made from rayon apparently affected her skin. Ammonia exposure causes her headaches and mental effects.
People stressed her and she would simply react to what came her way. If Ramona was ignored or insulted she did not know how to react and she and just complied with whoever produced this situation. Being ignored or insulted are areas of self-focus and since she had no self she shut down. Without a self you can be completely innocent and that is what attracted me to her and one of the reasons that I married her. Shortly after we married her sister asked her "do you only say what Nick says, don't you have any opinions of your own?" Ramona then came to me and asked if it was all right to just say what I {Nick} said. I told her she should have opinions of her own. This incident seemed to cause her to be become contrary in her behavior as she took my response as a command and therefore began reacting as though having opinions meant being contrary to me. Since she lacked insight and common sense I would was dumbfounded at her social blindness. Our interaction led me to ask her, "I guess you must think I read minds?" I was able to deduce things from social settings that were simply normal interactive perceptions; she was not. Her whole life was unfeeling patterns imprinted in her from others.
This set of articles needs to be read as interrelated as she exhibited many autistic traits, along with the continual cognitive deficits and "reality break" of schizophrenia, and some of the symptoms of Alzheimer's. That said, her condition was most like Autism. In certain primary ways it was like an inverted Autism in that she was locked into everything outside of self. Yet, I would not say it was any of these, but a condition unto itself. I have named it "Immunoinsanity". Her logic in conversation was often disjointed and ever since I have known her she had trouble with intimate eye contact. On occasion she would insult me out of the blue for no reason and at times strike me. I would tell her that she should not hit me and that it was not appreciated. Yet, she still did it on occasion. This behavior baffled me.
Wheat will still take her out of reality and drugs or substances that are phenolic effect her quite severely. These reactions are not obvious to the casual observer as she does not bite, kick or, scream. Yet it is clear her memory is affected, as is her reasoning ability. In her case of not knowing what having a self was is best summed up by the idea you don't know what you don't know. She remembered in a trivial way with everything standing alone having no relevance to other events or relationships in her life. She retained patterns and facts, but had no feeling or attachment that ever caused contemplation, reflection, or association. Basically she was a reflective machine that everyone liked because she reflected him or her and people generally like that. She never displayed any selfish motives although her behavior at times seemed very selfish. She never really hated or loved. For her it was not possible. She had no control. I have, since having understood her past condition, affectionately thought of her as the "human pinball".
I suspect that some damage or disorder had been occurring in her limbic system, and that her temporal lobes have been impacted as well. This was likely caused by a toxic phenol overload and/or a disruption of function of neurotransmissions by exogenous endorphins from undigested gluten, giladin, or casein called peptides. Because "peptides are the actual epitopes or immunolgically critical signals cut out from foreign proteins and presented to immunecompetent cells for antibody formation, it is possible that molecular mimicry occurred with cross reactivity towards endogenous proteins. On this premise one may envision antibodies attacking her brain receptors", other brain cells, or myelin and doing further damage.
It is also my contention that her dopamine levels were drastically out of control as phenylalanine is involved with dopamine levels. If her phenol-sulfotransferase pathway was deficient {this enzyme group metabolizes phenols, amines - which includes certain neurotransmitters, salicylates, and hormones} then the levels of dopamine production, uptake, and removal would be disturbed, as would other neurotransmitter and hormonal levels. Dopamine levels are suspected as a central factor in schizophrenia. The dopamine levels would then interact with other neurotransmitter levels {esp. serotonin} and create chaos in cognition and affective stability. In the near future she will undergo an EEG to try to determine if there is damage to her brain or if abnormalities exist. She is also getting ready to have a hair analysis done to measure the mercury levels in her body.
This paragraph deals with areas that I am just now looking into and am only considering the possibility of their involvement. I am wondering if HSV, cytomegalovirus, or other viruses may be present and have a role in her immune problems. Viruses that may produce encephalopathic or encephalitic effects are being considered. Certain viruses could possibly cause subcutaneous brain inflammation and account for her bulging eyes at times when she seems to have a viral infection. I realize this may be a result of her thyroid condition, but the timing suggests viral connections. Maybe any viral infection activates this condition or interacts with a latent virus. The immune modulator IVIG might be helpful in dealing with her immune system disorder, but that will be something considered more seriously down the road. An immunologic panel may be helpful in determining possible viral connections. I know something is very wrong with her immune system as she still has mental slowing and change {not just normal lethargy and irritability} whenever she gets a virus, not just when she eats the wrong foods. Although improved she still contracts illnesses more often than would be expected.
The problems here are so bizarre and complex that it may be hard for anyone who did not live with her and observe these traits and connections to understand or make sense of any of this as relating to each other or to anything. It's worth a try.

Nick 7/04/97 {edited since 7/04/97}
Addendum - On 7-11-97 Ramona also began taking l-carnitne. It is involved in fatty acid metabolism. It already seems to be helping, but a few more weeks of taking it is needed to be sure it is responsible for the additional improvement. I am also preparing to give her alpha-keto glutaric acid, which is a pre-cursor to carnitine production in the body. It also helps with cellular ammonia detoxification, among other things.
I can tell that the approach taken to deal with her condition has allowed her gastrointestinal functioning to greatly improve, but I still believe that there is room for more. A trial of betaine hydrochloric acid tablets to aid digestion and maintain a proper ecology will be given to her to see if any other benefits may be given her. Glutamine is also planned to help with intestinal healing. Methyl Sulfonyl Methane, or MSM is also planned. Update 9/16/97 - MSG {mono-sodium-glutamate} is harmful to her mental condition and Glutamine, in supplement form, may be.
Update 12/10/97 – Since Ramona was still having an acetone odor to her breath I suspected that she was not rid of her parasite problem and she began taking “Michael’s Paraherbs” on 11/27/97. Within a week she was passing worms and other odd looking {probably parasites} items that were visible in her stool. She is still passing worms. She also began taking Vitamin A in the form of cod liver oil and chelated iron. On 12/10/97 we received Ramona’s hair test which revealed a .007 lithium content {extremely low}, low manganese, disturbed mineral ratios, and a very high aluminum content. The mercury level was low, but I believe that the hair test may be unreliable regarding methyl mercury effects and levels. I am still studying the possible mercury connections. I believe a hair test result two years ago would have revealed far greater imbalances and deficiencies since many steps have been taken in the interim that undoubtedly have improved these conditions.
Continued 7-11-97
In the foreword I stated that Ramona had memories in second person and later I called her condition "Immuno Insanity". I was at a loss of how to relate what picture was forming as to the state of her mind and cognition, or lack thereof. I realize now that the second person statement is not helpful in conveying an understanding of the condition and maybe just inaccurate. I will try again.
The closest encompassing concept I have found and adapted is one taken from a theory about language and literature that developed in the 1970s. It is called deconstruction, and was proposed by Jacques Derrida. For the "coherent" individual I find the theory a convenient way to escape from objective realities, presuming one believes in such. It is therfore personally invalid, and only a nice reference point for distinguishing practical reality from chaos. To me chaos is where his theory ultimately leads. Yet for the incoherent mind, as was Ramona's, the theory is applicable. This application is made in the realm of her psyche.
"In the theory of deconstruction and for the deconstructionist, language is everything. What most characterizes deconstruction is its notion of textuality; a view of language as it exists not only in books, but also in speech, in history, and in culture. The world itself is "text." Language directs humanity and creates human reality. (A reality that cannot be named or described is illusory, at best.) Yet, upon close examination, words seem to have no connection with reality or with concepts or ideas."
The biological disruption in Ramona's brain produced chaos and a state of unreality. Her world was like this theory it had appearances of reason and connection to an outside interpreter {anyone around her}, but on closer examination her actions and words had no connection with reality or with concepts or ideas. This was true for her, yet it is hard for those without {the interpreters} to embrace such chaos without imputing reasoning, motives, and/ or will in their interpretation. That is how most "well" people react to mental illness when they see it in others. In Autism an explanation called "Theory of Mind" is used to explain the disturbed or chaotic mind. In general mental illness (Autism is not a mental illness} is explained by terms like psychosis and dementia. Yet, even in these understood terms the interpreters have no way to really empathize with someone with mental problems. If one had severe problems themselves and recovered they might understand the plight. Even so, Ramona cannot make sense of what happened in her mind. She did not have dementia she had amentia.
With the deconstruction concept in mind I have found a better descriptive and more sophistric name to describe her past condition. The better name is "MIND syndrome" or "MINDS". This stands for "Metabolic Immuno Neurologic Deconsrtuction Syndrome."
Now that Ramona has made such dramatic improvement I have observed another interesting trait in her. She has a completely uncontrollable "startle response" when looking me in the eye. Even if she is prepared and knows I am going to attempt to startle her if she is looking me in the eyes, a quick motion or moderate to loud sound will cause her to flinch. She often has an attendant rush of adrenaline at these moments. Under certain conditions she can even startle herself while making noises. This has happened when she was doing a task at the same time that she was being vocally expressive in a dynamic way. It was tied to being spontaneous. It is likely that while she was in her previous condition she probably had some paralyzing responses to such stimuli, but had no mental capacity to connect to an outward startle reaction. This would have been reflexive, and not consciously suppressed or understood.

This was the bringing, light years of understanding have passed.



I am working on submitting more relevant information, but this is rehab for me. Bless AoA.

Can You Feel The Love Tonight (The Lion King) - Elton John (Boyce Avenue ft. Connie Talbot cover)



Truth It means all or nothing.



I have loved ABBA before there was Madonna

Madonna ended up ‘begging’ Abba to use sample
Madonna has revealed that she wrote a letter to the members of ABBA begging to use their music on one of her tracks.

The star wanted permission to sample the Swedish pop titans’ massive 1979 disco hit ‘Gimme, Gimme, Gimme (A Man After Midnight)’ for her latest single ‘Hung Up’, out on November 7.

Songwriters Benny Andersson and Bjorn Ulvaeus very rarely allow other artists to use their tracks.

Speaking to Attitude magazine, Madonna said: “I had to send my emissary to Stockholm with a letter and the record begging them and imploring them and telling them how much I worship their music, telling them it was an homage to them, which is all true.

“And they had to think about it, Benny and Bjorn. They didn’t say yes straight away. They never let anyone sample their music. They could have said no. Thank God they didn’t.”

Andersson was recently quoted as saying: “We get so many requests from people wanting to use our tracks but we normally say no. This is only the second time we have given permission.”


Gavin Newsom, I hold out hope for the Democrats of my Father. I will watch and wait.



Its a start. Yet amateurs.

Inflammation and Mental Health Symptoms

"New research provides some of the first experimental evidence that inflammatory processes influence our decisions. The findings, which appear in the journal Adaptive Human Behavior and Physiology, suggest that factors that promote inflammation may also contribute to impulsivity.

“We initially became interested in this topic after beginning to explore the role of the body’s condition (e.g., hunger, health, etc.) on decision-making in a variety of domains, like interpersonal processes, risk-taking, and impulsivity,” said study author Jeff Gassen, a doctoral candidate at Texas Christian University and member of Sarah Hill’s Evolutionary Social Psychology Lab.

“We developed a hypothesis that the immune system may play an important role in calibrating individuals’ behavior to their bodily state, given that the immune system both monitors the state of the body and can communicate with the brain. Specifically, inflammation increases when the body is threatened or in poor condition, a time when an individual needs to invest in what’s going on right now (whether it be rewards, opportunities, or taking steps to recover) and think less about the future.”

The researchers were specifically interested in the relationship between pro-inflammatory cytokines and delay discounting. Cytokines are proteins produced by the immune system, while delay discounting is the tendency to take a smaller reward that is available immediately rather than a larger reward that will be delivered in the future.

“So, we predicted that inflammation may play a mechanistic role in increasing present focus. We also have a recent paper published in Scientific Reports, that outlines our theoretical model in more detail,” Gassen said.



My Testimony.

No Longer Visiting

I Deserved This….I Didn't Deserve This. Vale


I suppose I have almost come full circle. Having sought through science a satisfying and complete enough explanation it has always been missing any real point. Since I am one who believes in revelation of the Divine it, the experience and knowledge this journey has supplied, should fit somehow. I am not demoting science it just lacks some things. Many may find this absurd, and I am only suggesting possible validity for what is on the page linked. A few posts back I linked Sam Cooke's "Touch the Hem of His Garment". I finally am discerning some Providence again in my trial and journey.



I quite like music and freedom, but the girl in the bathtub makes me consider trading both for sanity..
The trade would not acquire love or truth though.



Where is my Madonna Vogue link?
Intelligent woman



Two steps forward.


I think I have followed Penrose and Hameroff from when they first published in the 90's. I have to say I hope there is something to their ideas. It is what it is.

Microtubules and human consciousness


I have not reached the end of my understanding as one can always learn something new. Weariness is powerful.


I almost never swear and disavow its use in an earlier post. Microtubules and the quantum world? Maybe some wonderful music there too? Micro tubules are not discussed in the article, yet one could speculate.

The Good Vibrations of Quantum Field Theories

"Quantum fields are really a mind-bending way of thinking. Everything—and I mean everything —is just a consequence of many infinitely-large fields vibrating. The entire universe is made of fields playing a vast, subatomic symphony. Physicsts are trying to understand the melody."



I have traveled to the end of f my understanding and sanity and the arrows end up pointing a certain way. I must needs go home. My apologies to any expecting another reality. My honest conclusion. My sister says she was born into an ocean of love. We both were. Praise God.



I don't know who she really is, but she goes by Lady Ga Ga. Condensing complexity into a phrase and simple melody is the sign of pure love and genius. So touching and human. God speaks.



Thanks Hans, I had not returned to find what you have reported though some of the information is accurate as to processes. {Should be nonplussed a couple of posts back as when myself I fully know., I have to get a grip on this though the madness of this who0le experience has screwed with my head.)

Hans Litten

"Are you familiar with the website ?" "https://epiphanyasd.blogspot.com/"
I have been through the things there yeas before anyone discussed the matter.

Posted by: Visitor | April 20, 2019 at 05:59 PM

They are a pro-pharma run group. Out of the former Yugoslavia region. Peter somebody.
What is contained may sometimes very well be valid however they launched a vicious attack denouncing the Geiers & defended intravenous mercury which is just incredible.
They are a pro-vaccine team and they think autism came down with acid rain.
I had it with them, they have got nothing in reply. And have never returned.


The sad things is people are not usually moved from intrinsic agreement and await external validation..
God is immanent ready to move with a spirit. The spirit is excluded and becomes dependent on the physical.
God is preempted in favor of groupthink.


Saw Avengers' Endgame Saturday. Glorious! So good! They included a song I absolutely love from my teens. I had played this song for my children some years ago and they were not plussed. Since they are Avengers fans and it is in the movie I suspect they may change there tune.
Rubber Band Man - How can this not move someone?

They also included this gem.



This remains.


To understand in the face of utter ignorance makes me to want to put a gun to my head and blow my fucking brains out! I am serious the ignorance is unbelievable!


If any consider my story they may think I helped my wife, but ultimately it was just Jesus passing through involving generations before me..




God is perfect t. I am blessed to know He is. Some will dismiss this. God is all. God is more than good.


I can't contain my appreciation for Bob Moffit. God bless you. Also I absolutely love Kin and Teresa. Conrick. Such strong and beautiful people that show God to me. Teresa, I am with you in spirit, keep going.


In mice, eliminating damaged mitochondria alleviates chronic inflammatory disease. I have felt and known this, and don't don't know what connection this has to: "It is finished". Bless the Lord Jesus I am trying..


I don't know what the point is.





"It's amazing how music calls on different parts of the brain than logical thinking does."



There must be a thread of humanity.


Those who want to force vaccination are my mortal enemies. Where are the damn liberals!!!


Reason and logic are honest, but useless.



Sultans of immune disruption. Kicking against the establishment.


I have studied the hell out of this,

I think I will offer more.




Release for loving people. Bless each of you.



I will likely not be remembered for much. I have been open to what is occurring in life, God and faith have waxed and waned in my life for many years. The incidents have meaning, but always eventually wane. What seems to hit me in the face id God's grace. I know of proteins and pathologies, but God is Love.



I am not all that secure and make statements that I think better of after I recover. This being a last post is one. This link and info speaks of things I found some years before this was posted and I would add depending on the case there may be much more involved as in epigenetics or other gene effects. Yet, here is some aspect of what is involved in what is diagnosed as autism in may cases.

The Underlying Mechanisms of Brain Allergies


"A connection between mood and the immune system has been suggested, with brain chemistry as the link. Ader suggests that the limbic system is where chemical messengers from the immune system have action.1 Felten noticed that the autonomic nervous system can be affected by emotions; in particular, insulin and blood pres-sure regulation. He also discovered synapse-like contacts linking the auto-nomic nervous system with lymphocytes and macrophages.2 Apparently, neuro-transmitters regulate immune cells.

The most vulnerable place in the brain for immune signal effects is the hypo-thalamus because it lacks a blood brain barrier (BBB). During a cold, the hypo-thalamus receives cytokine stimulation that alters homeostatic set points leading to fever, loss of appetite, insomnia and dia-phoresis. Even the common cold can make a person feel irritable, restless, achy, and down. One might assume that humoral cytokines and histamines would not enter other brain structures because of protec-tion by the BBB but that assumes that the integrity of the BBB is intact. Some people may have compromised barriers leaving them with more widespread effects of unwelcome substances.3


The elucidation of synaptic transmis-sion as the means of neuronal communi-cation in the brain was revolutionary. It is convenient to think of the synaptic event as a packaged phenomenon, but neuro-transmitters are not selective, their receptors are. The distribution of receptors and synaptic vesicles for specific neuro-transmitter substances do not correlate well within regions of the brain. Less than two percent of neuronal communication actually happens at the synapse.4 A neuro-transmitter substance can bind a postsynaptic receptor, bind a presynaptic auto-receptor, be degraded by enzymes, be taken up presynaptically, or diffuse into the environment of the brain until it can influence receptors distal to the site of release. In other words, the brain’s communication system resembles the endocrine system. This concept opens up a wide range of possibilities for chemical influences at various sites in the brain.

Endocrine and immune influence on the mind occurs via receptors present on brain tissue. The brain has receptors for sex hormones. In utero, the developing brain is gender specific under the influence of estrogen and testosterone.5 The release of certain neuropeptides may be modulated by feedback mechanisms. For example, thyrotropin releasing hormone is upregulated by dopamine and down-regulated by serotonin.6 Histamine, a common secretion of immune activity, has at least three types of receptors to choose from in the brain.7 Histamine is now being recognized as a neuoractive amine on top of its role in the rest of the body. Furthermore, hormones and cytokines have effects on the enzymes controlling brain communicating sub-stances. For example, conjugated estrogen inhibits monoamine oxidase activity thereby elevating mood.8

Allergic Reactions

Symptoms: Adverse reactions from food are usually termed “food allergy” if it is histamine related or “food hypersensitivity” if it is otherwise. Allergic reactions to food exposure can range from the very mild, as in hives, to severe, the most serious being anaphylaxis. That type of response, however, is not the focus of this discussion, which intends rather to explore the “masked allergy” that may or may not involve the immune system directly but does have an impact on brain’s function: i.e., food intolerance that slowly inhibits wellness.

What Pfeiffer called the “allergy-tension-fatigue syndrome” involves a variety of symptoms ranging from hyperactivity to somnolance. The most commonly incriminated foods are cow’s milk, wheat, beef, bananas, chocolate and sugar. The neurological symptoms he noticed in his patients when they ate some of these foods in-cluded:"


Candida infection can reach brain and impair memory

"A new study in mice reveals that Candida albicans — a fungus largely perceived as harmless — can cause memory problems and brain abnormalities that resemble those characteristic of Alzheimer's disease.

scientist regrafting bacteria

C. albicans is the most common and best-studied cause of fungal infections in humans.

Candida albicans is a species of fungus that grows naturally in the human gut, mouth, and vagina.

Although the yeast is mostly harmless, it can develop into issues ranging from thrush to more serious infections that reach the blood and other organs.

C. albicans is the most common cause of fungal infections in humans, as well as the most extensively studied fungal pathogen that affects people.

A new study, which appears in the journal Nature Communications, adds to the existing body of knowledge about C. albicans.

The new research shows that the fungus can enter the brain, trigger an inflammatory response, and impair memory in mice.

Importantly, the infection leads to the formation of abnormal structures in the brain, and these share similarities with amyloid plaques — a hallmark of Alzheimer's disease.

Dr. David B. Corry, a professor of medicine-immunology, allergy, and rheumatology at the Baylor College of Medicine in Houston, TX, is the corresponding and final author of the new study.

Finally, the scientists decided to inject a dose of 25,000 yeasts in the rodents' bloodstream. Dr. Corry and the team were surprised to discover that the fungus penetrated the blood-brain barrier.

The blood-brain barrier is a mechanism that protects the brain from pathogens that may exist in the blood. The barrier separates the brain's capillaries, or blood vessels, from the brain's cells and tissue.

C. albicans crossed this barrier and affected the brain's immune cells. "We thought that yeast would not enter the brain, but it [did]," comments Dr. Corry.

"In the brain, the yeast triggered the activity of microglia, a resident type of immune cell," he explains, adding, "[t]he cells became very active, 'eating and digesting' the yeast. They also produced a number of molecules that mediated an inflammatory response, leading to the capture of the yeasts inside a granule-type structure inside the brain."


Two Foods That May Sabotage Your Brain


music for souls

Bradley Cooper - Maybe It's Time


What Will Become of Us - Phillip Phillips









This is a good foundation that I need to accept.


Forgot the link to add the last abstract.











Some Science of the Soul {from a sinner}



interesting visitor.




CCL2 (MCP-1)
CCL4 (MIP-1)
CCL17 (TARC)[8]
CCL22 (Macrophage-derived chemokine)[9]



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