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

"The one thing about my husband and I...we laugh...A lot. We find a way. We really do. Poop filled sleepless nights, injuries, missed appointments, clutter everywhere, missing paperwork...sometimes all you can do is laugh. But today, looking at the dark circles we've seen so many times under our children's eyes, seeing the suffering, the real genuine human suffering that we have worked for three years to alleviate...to see it reach these depths...there is no laughing today. There is sadness. Even the fight is gone. I should be sleeping, but I have to read up on one of our new remedies. Maybe this will be the one that touches his immune damage and regulates him? Maybe. Maybe, it will work for him like it has for THOUSANDS of other children. Maybe. I can't sleep when this could be it and I could be calling the next doctor tomorrow and we could have one less day of this. Plus, I already have an appointment to see a doctor tomorrow and I will need him to know that I know what I'm talking about. If there is one thing you learn as an autism parent it is that YOU MUST KNOW WHAT YOU ARE TALKING ABOUT WITH DOCTORS. You must learn to speak their language. If you don't you will get dismissed. Must read, now.



But, before I go, just need to let everyone know the women who work for us are angels from God. They were hurt today. Two of them. In their sweetest voices they kept repeating, "nice hands." And "time to get down monkey" when he climbed on the counter for the 27th time on their shift. He is 50 lbs now. Very fast and very strong. They get him. They see the real Noah in there, fighting like hell. He is mad. In fact, that's what he said in therapy today, "I'm MAD!" His therapists were thrilled. They were so excited to see him emote appropriately. I agree with them, it's encouraging. It's just that, he's mad he's sick. He's mad his head hurts all the time. He's mad his three year old brother can use the toliet and he cannot. He's mad that his body is rebelling against him and everything hurts. He's mad that in addition to not getting to go where everyone else goes and doing all the fun things other 5 year olds do, he also cannot EAT anything they do. It seems cruel doesn't it? It is.

Autism is the cruelest most malicious, devious, conniving, heinous disease. If you fear the chicken pox or diarrhea more you are in big, big trouble. Because I guarantee with the new schedule autism will come a knocking at your door. And it will get in. It finds a way. Sometimes it looks like OCD, sometimes it looks like ADHD, even arthritis. "That's nuts!", you say. Not really. It should all just be called autism. Because any time pharma causes inflammation they don't want you to find out about, they just make up a word for it. Autism. Asthma. ADD. Just made up words for inflammation. Off to read ABOUT AUTISM . It's a good one, you might want to check it out yourself... Much hope for all our beautiful children. xo lj "

Lisa Goes is Contributing Editor to Age of Autism.

Comments

Visitor

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.

Abstract

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.

https://www.ncbi.nlm.nih.gov/pubmed/3890202

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

Abstract

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.

https://www.ncbi.nlm.nih.gov/pubmed/31009952

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

Abstract

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.

https://www.ncbi.nlm.nih.gov/pubmed/26052927

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.

Abstract

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.

https://www.ncbi.nlm.nih.gov/pubmed/29497932


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

Abstract

SETTING:

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.

OBJECTIVE:

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

DESIGN:

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

RESULTS:

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.

CONCLUSION:

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.

https://www.ncbi.nlm.nih.gov/pubmed/31697922

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

Abstract

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.

https://www.ncbi.nlm.nih.gov/pubmed/21130154

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

Abstract

OBJECTIVE:

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.

RESEARCH DESIGN AND METHODS:

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.

RESULTS:

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.

CONCLUSIONS:

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.

https://www.ncbi.nlm.nih.gov/pubmed/31601636

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

Abstract

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.

https://www.ncbi.nlm.nih.gov/pubmed/28415925

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

Abstract

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.

https://www.ncbi.nlm.nih.gov/pubmed/20628445

Visitor

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."

https://www.spectrumnews.org/news/surplus-of-immune-cells-may-mark-brains-of-autistic-people/

Visitor

hmmm...familiar actors

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

OBJECTIVE:

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.

METHODS:

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.

RESULTS:

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.

CONCLUSION:

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.

https://www.ncbi.nlm.nih.gov/pubmed/15934096

Visitor

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

https://link.springer.com/article/10.1186/s11689-019-9268-y

Visitor

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.

Abstract

"Activity-dependent neuroprotective protein (ADNP), discovered and first characterized in our laboratory (IG), is vital for mammalian brain formation and presents one of the leading genes mutated de novo causing an autistic syndrome, namely the ADNP syndrome. Furthermore, a unique mouse model of Adnp-haploinsufficiency was developed in the laboratory (IG), with mice exhibiting cognitive and social deficiencies. ADNP is regulated by vasoactive intestinal peptide (VIP), and pituitary adenylate cyclase-activating peptide (PACAP). In this respect, PACAP was independently identified as a sexual divergent master regulator of the stress response. Here, we sought to determine the impact of the Adnp genotype and the efficacy of PACAP pre-treatment when subjecting Adnp+/- mice to stressful conditions. Significant sex differences were observed with Adnp+/- males being more susceptible to stress in the object and social recognition tests, and the females more susceptible in the open field and elevated plus maze tests. Splenic Adnp expression and plasma cortisol levels in mice were correlated with cognition (male mice) and anxiety-related behavior. These findings were further translated to humans, with observed correlations between ADNP expression and stress/cortisol content in a young men cohort. Altogether, our current results may establish ADNP as a marker of stress response."

https://www.ncbi.nlm.nih.gov/pubmed/31534115

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

Abstract

"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."

https://www.ncbi.nlm.nih.gov/pubmed/17952637

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

https://www.ncbi.nlm.nih.gov/pubmed/17952636

Helpful to read.
Vasoactive intestinal peptide

https://en.wikipedia.org/wiki/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.

Abstract

"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."

https://www.ncbi.nlm.nih.gov/pubmed/22375693

Heard Magnesium Sulfate for some Autism?

Intravenous magnesium sulfate rapidly alleviates headaches of various types.

https://www.ncbi.nlm.nih.gov/pubmed/8984087

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

https://headachejournal.onlinelibrary.wiley.com/doi/abs/10.1111/j.1526-4610.2012.02214.x

Visitor

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
https://rgd.mcw.edu/rgdweb/genes/mirnaTargets.html?id=2299183&fmt=full

CCND1 Gene

https://www.genecards.org/cgi-bin/carddisp.pl?gene=CCND1

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

https://www.ncbi.nlm.nih.gov/pubmed/31664177

ADNP Gene

https://www.genecards.org/cgi-bin/carddisp.pl?gene=ADNP

Visitor

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.

https://www.extremetech.com/extreme/300458-neanderthal-denisovan-dna-found-near-autism-genes-in-modern-humans

https://arstechnica.com/science/2019/10/long-stretches-of-neanderthal-and-denisovan-dna-helped-homo-sapiens-adapt/

https://www.genecards.org/cgi-bin/carddisp.pl?gene=EPAS1

https://www.genecards.org/cgi-bin/carddisp.pl?gene=TNFRSF10D

https://www.genecards.org/cgi-bin/carddisp.pl?gene=TIMP3

Migraine
https://www.genecards.org/cgi-bin/carddisp.pl?gene=TRPM8&search=trp-p8

https://www.youtube.com/watch?v=xdRHSuPxgXo

Visitor

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.

https://cosmosmagazine.com/biology/immune-system-lends-a-hand-to-the-brain

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

https://immunology.sciencemag.org/content/4/40/eaay5199

Visitor

James Taylor - Something In The Way She Moves

https://www.youtube.com/watch?v=Bfk9nvUni88

Visitor

Not a surprise. Very glad this was studied.

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

Abstract

"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."

https://www.ncbi.nlm.nih.gov/pubmed/31502418

Visitor

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."

https://www.sciencedaily.com/releases/2019/08/190829102816.htm

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.

Abstract

BACKGROUND:

"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.

METHODS:

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.

RESULTS:

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.

CONCLUSION:

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."

Copyright© Bentham Science Publishers; For any queries, please email at epub@benthamscience.net.

https://www.ncbi.nlm.nih.gov/pubmed/31456514

Visitor

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

https://www.intechopen.com/online-first/innate-immunity-and-neuroinflammation-in-neuropsychiatric-conditions-including-autism-spectrum-disor

Visitor

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

https://www.youtube.com/watch?v=k_NJ2Nzf_Qk&list=OLAK5uy_lUDoJV5KpgPkG5nFwFK2iAxCc_yeI164s&index=13

Visitor

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

https://www.mdpi.com/1099-4300/15/1/372/htm

Visitor

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.

http://www.ncbi.nlm.nih.gov/pubmed/22729468

If 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."

https://www.technologynetworks.com/neuroscience/news/neuroscientists-identify-surprising-brain-action-of-cartilage-component-hyaluronic-acid-322048

Visitor

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.

Visitor

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.

https://www.youtube.com/watch?v=ZEWGyyLiqY4

Visitor

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.

Notebook
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."
9-25-97
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.
Nick

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

https://www.youtube.com/watch?v=esrTfwBiOM0


Visitor

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)

https://www.youtube.com/watch?v=1sioip9Uc4o&list=PL0BD69368AB943C89

Visitor

Truth It means all or nothing.

https://www.youtube.com/watch?v=_YC3sTbAPcU

Visitor

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.”

https://www.nme.com/news/music/madonna-270-1319586

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

https://upload.wikimedia.org/wikipedia/commons/thumb/7/70/Jfk2.jpg/1024px-Jfk2.jpg

Visitor

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.

https://www.psychologytoday.com/gb/blog/expressive-trauma-integration/201905/inflammation-and-mental-health-symptoms

https://www.youtube.com/watch?v=gNarAFhOw1I

My Testimony.

No Longer Visiting

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

Visitor
Visitor
Visitor
Visitor

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.

http://www.esotericmeanings.com/crucifixion-allegory-part-2/

Visitor

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.


https://www.youtube.com/watch?v=diYAc7gB-0A

Visitor

Where is my Madonna Vogue link?
Intelligent woman

https://www.youtube.com/watch?v=GuJQSAiODqI

Visitor

Two steps forward.
https://www.youtube.com/watch?v=27RVIgW7L8c

Visitor

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

https://excal.on.ca/microtubules-and-human-consciousness/

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

Visitor

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."

https://www.pbs.org/wgbh/nova/article/the-good-vibrations-of-quantum-field-theories/

Visitor

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.

https://www.youtube.com/watch?v=pn12xo2Dwas

Visitor

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.

https://www.youtube.com/watch?v=_vR32XI3Sr4

Visitor

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.

Visitor

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.

Visitor

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?
https://www.youtube.com/watch?v=Y1BX9VWMP7c

They also included this gem.

https://www.youtube.com/watch?v=EHcsuiKgg0U

Visitor

This remains.
https://www.youtube.com/watch?v=O94CW_tIEzU

Visitor

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!

Visitor

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

Visitor

https://www.youtube.com/watch?v=xaSmjdWEK9E

Visitor

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

Visitor

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.
https://www.youtube.com/watch?v=O94CW_tIEzU

Visitor

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..

https://www.sciencedaily.com/releases/2019/04/190411154722.htm

I don't know what the point is.

Visitor

"Are you familiar with the website ?" "https://epiphanyasd.blogspot.com/"

I have been through the things there yeas before anyone discussed the matter.

Visitor

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

Visitor

https://www.youtube.com/watch?v=oag1Dfa1e_E

There must be a thread of humanity.

Visitor

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

Visitor

Reason and logic are honest, but useless.

https://www.youtube.com/watch?v=x0RV0kgdqJU

Visitor

Sultans of immune disruption. Kicking against the establishment.

https://www.youtube.com/watch?v=x0RV0kgdqJU

I have studied the hell out of this,

I think I will offer more.

Visitor

https://www.youtube.com/watch?v=bo_efYhYU2A

Visitor

Release for loving people. Bless each of you.

https://www.youtube.com/watch?v=k_X2S2dXcjk

Visitor

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.

https://www.youtube.com/watch?v=_vR32XI3Sr4

Visitor

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

Psychoneuroimmunology

"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

Psychoimmunoendocrinology

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:"

http://orthomolecular.org/library/jom/2000/articles/2000-v15n01-p005.shtml


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."

https://www.medicalnewstoday.com/articles/324106.php

Two Foods That May Sabotage Your Brain

https://kellybroganmd.com/two-foods-may-sabotage-brain/

music for souls

Bradley Cooper - Maybe It's Time

https://www.youtube.com/watch?v=RdljoTFMhO4

What Will Become of Us - Phillip Phillips

https://www.youtube.com/watch?v=BhFlWoSHQ1s

Visitor

I don't know what to make of the whole 9 yards. I have studied many issues for over 20 years and find that it made sense in many ways "scientifically "yet all of this has a dimension that I don't comprehend. I will simply offer my apologies for intruding into this effort and also for my comments made when I was not in my right senses. These comments may sound measured, but I am very perplexed to put it mildly. Off and on there seemed to be more than there appeared though the notion was too incredible to integrate to my reality. . I believe this is my last post here. Thank any who have attempted to assist.

Visitor

https://www.youtube.com/watch?v=lgXW6XDnhXA

Visitor

Please indulge this and me as God is first or should be if it means anything.. After a lot of work grace is the answer.

"Love says: I am everything. Wisdom says: I am nothing."

This is a good foundation that I need to accept.

Visitor

Forgot the link to add the last abstract.

Analysis of neurodevelopmental delay in children exposed in utero to hyperemesis gravidarum reveals increased reporting of autism spectrum disorder

https://www.sciencedirect.com/science/article/pii/S0890623818305586?via%3Dihub

Visitor

Like to read the whole report, though have already surmised this. Search back this thread if interested.

Analysis of neurodevelopmental delay in children exposed in utero to hyperemesis gravidarum reveals increased reporting of autism spectrum disorder


Highlights


• Neurodevelopmental diagnoses in children exposed to Hyperemesis Gravidarum were compared to diagnoses in unexposed children.
• Hyperemesis Gravidarum may be associated with a 3-fold increase in odds of having a neurodevelopmental diagnosis ∼age 12.
• 8% (22/267) of children exposed to HG in utero were reported by mothers to have an autism spectrum disorder (ASD) diagnosis.
• None (0/93) of the unexposed children were reported by their mothers to have ASD.
• As early intervention for ASD can be critical to prognosis, larger studies are urgently needed to confirm the findings.

Abstract

"The purpose of this study was to follow up on the reporting of neurodevelopmental disorders in children exposed in utero to Hyperemesis Gravidarum (HG). This was an exploratory descriptive study whereby neurodevelopmental outcomes of 267 children delivered by 177 mothers with HG were compared to neurodevelopmental outcomes from 93 children delivered by 60 unaffected mothers. Similar to at age 8, the children (now 12) exposed in utero to HG had over 3-fold increase in odds of neurodevelopmental disorders including attention, anxiety, sensory, sleep difficulty, and social development delay/social anxiety. However, with the longer follow-up, there was also a significant increase in Autism Spectrum Disorder (ASD), reported in 22/267 (8%) of children exposed to HG in utero and no unexposed children. As early intervention for ASD can be critical to prognosis, larger studies are urgently needed to determine whether ASD is associated with exposure to HG."

Visitor

Some Science of the Soul {from a sinner}

https://www.youtube.com/watch?v=Rak_rJLG49k

greyone

interesting visitor.
Dr Horowitz had a slide about chemokine signature for borreliosis infections about 17:30 in this lecture at lymeMIND
https://m.youtube.com/watch?v=kdJPQgAkxF0

Visitor

An additional part from the Wiki entry on CCR4 I quoted a bit from about chemokines involved mentioned in the last post I should have added this. Sometimes I assume people are seeing the things I find naturally involved. This pertains to the angiogenesis I have been highlighting in this thread as it relates to CCR4/CCL17. I will just repost what I did before plus the last paragraph added.

"The protein encoded by this gene belongs to the G protein-coupled receptor family. It is a receptor for the following CC chemokines:

CCL2 (MCP-1)
CCL4 (MIP-1)
CCL5 (RANTES)
CCL17 (TARC)[8]
CCL22 (Macrophage-derived chemokine)[9]

"Chemokines are a group of small structurally related proteins that regulate cell trafficking of various types of leukocytes. The chemokines also play fundamental roles in the development, homeostasis, and function of the immune system, and they have effects on cells of the central nervous system as well as on endothelial cells involved in angiogenesis or angiostasis.[7] "

https://en.wikipedia.org/wiki/CCR4

Visitor

The irresistible CCL17

New role for the allergy driver: It influences signal transmission in the brain

"The chemotactic protein CCL17 attracts immune cells to where they are currently needed. Doctors have long known: A high level of this substance in the body indicates an allergic reaction. A team of scientists led by the University of Bonn has now discovered a completely new function: CCL17 also influences signal transmission in the brain. There may even be a molecular link to autism. The results have now been published in the journal Glia.

Chemotactic cytokines, chemokines for short, are signaling proteins that act like an attractant and ensure, for example, that immune cells migrate from the bloodstream into the tissues. The chemokine CCL17 is known to increase inflammation and is associated with allergic diseases. A high level of CCL17 in the blood is regarded by doctors as a diagnostic marker of ongoing allergic reactions such as atopic eczema. The further the research on chemokines progresses, however, the more functions are discovered. Thus, an earlier joint study by the Universities of Münster and Bonn showed that animals with a defect in the expression of the receptor for CCL17 have behavioral problems: For example, they were unable to build proper nests like their normally developed mates.

"These behavioral changes indicated that CCL17 not only affects the immune system but perhaps also the brain," explains the corresponding author of the study, Prof. Dr. Irmgard Förster from the LIMES Institute at the University of Bonn, who is also a member of the Cluster of Excellence "ImmunoSensation." If there is such a connection, which cells in the brain produce CCL17? This question was investigated by doctoral student Lorenz Fülle and Irmgard Förster, together with scientists from the Institute of Cellular Neurosciences around Prof. Dr. Christian Henneberger, Dr. Annett Halle from the German Center for Neurodegenerative Diseases (DZNE) and Dr. Judith Alferink from the University of Münster.

Through a genetic modification, the researchers coupled the release of CCL17 with the production of a fluorescent dye that illuminated all cells that produce the chemokine. The scientists additionally stimulated CCL17 production by simulating an infection using a substance contained in bacterial cell membranes. The production sites of the chemokine in the brain were then clearly visible under the microscope. "CCL17 is mainly produced by neurons of the hippocampus," reports lead author Lorenz Fülle. This structure, which is shaped like a seahorse, is present on the right and left side of the brain, and fulfills an important function in tasks such as orientation and memory formation.

Scientists blocked the gene for CCL17

As a next step, the scientists blocked the gene for CCL17 production and observed the effect. In the absence of the chemokine, the microglial cells in these "knockout" mice were significantly smaller and there were only half as many as in untreated control animals. Microglial cells have long been known as immune cells of the brain, where they take responsibility as "health guards" for the disposal of cell debris and infectious agents. Meanwhile, it has been shown that these "scavenger cells" also directly support the work of the neurons independently of their phagocytic activity.

In order to investigate the effect of CCL17 on the function of neurons, scientists in the laboratory of Prof. Dr. Christian Henneberger at the Institute of Cellular Neurosciences (University of Bonn Medical School) examined neuronal signaling in the brain. Henneberger: "The experiments indicate that CCL17 attenuates signal transmission in the hippocampal region of the brain." Since autism in humans is also associated with elevated levels of CCL17 in the blood, CCL17 could also play a role in this developmental disorder, for example due to an infection or an allergic reaction in early childhood. "But so far these are speculations," says Förster. "The exact effects of CCL17 have yet to be demonstrated by further research."

https://www.sciencedaily.com/releases/2018/09/180913082142.htm

The C-C Chemokines CCL17 and CCL22 and Their Receptor CCR4 in CNS Autoimmunity.

"The C-C class chemokines 17 (CCL17) and 22 (CCL22) and their C-C chemokine receptor 4 (CCR4) have been shown to play an important role in homeostasis and inflammatory responses. Here, we provide an overview of the involvement of CCR4 and its ligands in CNS autoimmunity."

Here is some info from a report I posted here in 2013.

Elevated serum levels of macrophage-derived chemokine and thymus and activation-regulated chemokine in autistic children

"Background

In some autistic children, there is an imbalance of T helper (Th)1/Th2 lymphocytes toward Th2, which may be responsible for the induction of the production of autoantibodies in these children. Th2 lymphocytes express CCR4 receptors. CCR4 ligands include macrophage-derived chemokine (MDC) and thymus and activation-regulated chemokine (TARC). They direct trafficking and recruitment of Th2 cells. We are the first to measure serum levels of CCR4 ligands in relation to the degree of the severity of autism...

Conclusions

Serum levels of CCR4 ligands were elevated in autistic children and they were significantly correlated to the degree of the severity of autism. However, further research is warranted to determine the pathogenic role of CCR4 ligands in autism and to shed light on the therapeutic role of CCR4-ligand antagonism in autistic children."

https://www.jneuroinflammation.com/content/10/1/72/abstract

CCR4 -Wiki

The protein encoded by this gene belongs to the G protein-coupled receptor family. It is a receptor for the following CC chemokines:
CCL2 (MCP-1)
CCL4 (MIP-1)
CCL5 (RANTES)
CCL17 (TARC)[8]
CCL22 (Macrophage-derived chemokine)[9]

https://en.wikipedia.org/wiki/CCR4

John Stone

Visitor

This is probably a technical problem to do with the updating of the platform (which has been going on an annoyingly long time).

Visitor

Regarding the last [post, it also brings up "This site is not secure. If you simply copy the link address and paste it in to a browser address bar it will bring up the report. It seems to not be willing to link from this host.

Visitor

I posted a link to a report in the last post. Upon clicking on it now it says "This site is nor secure" and shows no report.

Here is the updated link to that report.

p38α MAPK signaling drives pharmacologically reversible brain and gastrointestinal phenotypes in the SERT Ala56 mouse

http://www.pnas.org/content/115/43/E10245

Visitor

Don't know where to start, but here is a thing I had been into a few years back on this thread about
p38α MAPK. This is mitochondrially related.

Scientists pinpoint pathway that impacts features of autism

https://medicalxpress.com/news/2018-10-scientists-pathway-impacts-features-autism.html
the report on this release

p38α MAPK signaling drives pharmacologically reversible brain and gastrointestinal phenotypes in the SERT Ala56 mouse

http://www.pnas.org/content/early/2018/10/03/1809137115

https://en.wikipedia.org/wiki/MAPK14

Autophagy in inflammation: the p38α MAPK-ULK1 axis

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5933864/

p38 MAPK inhibits autophagy and promotes microglial inflammatory responses by phosphorylating ULK1.

https://www.ncbi.nlm.nih.gov/pubmed/29196462

Visitor

So many songs filled with wisdom. They rarely provide answers, but they are genius in asking sustaining questions. AoA is a defining pulse.

Visitor

Having posted elsewhere on the sight on my view that the mother's microbiome and related immune(esp il-17} and system response influence Autism generation/risk and the pre natal health of the child, I though this piece gives some light. This is one particularly notable quote below.

TH17 cells in human recurrent pregnancy loss and pre-eclampsia

Systemic and local priming of TH17 cell differentiation in pregnancy
"Several differentiation factors and transcription factors that are unique to TH17 cells have been identified, marking TH17 cells as an independent subset of T helper cells. TGF-beta and IL-6 have been reported as the minimal requirements in mice for TH17 cell differentiation from naive CD4+ T cells; in contrast, IL-1beta plus IL-6 or IL-23 are required in human TH17 cells.47,48,49,50,51,52 IL-23/IL-23R plays an important role in stabilizing and endowing TH17 cells with pathogenic effector functions, that are regulated by serum glucocorticoid kinase 1.53 Compared with other TH lineages, including TH1, TH2 and Treg cells, TH17 cells have unique genetic programs to express the transcription factor RORgt, which induces the transcription of the Il17A gene.8 Other transcription factors, such as STAT3,54 RORalpha55 and interferon regulatory factor 4,56 have been reported to be important in TH17 differentiation. Aryl hydrocarbon receptor, an environmental toxin sensor, has also been identified as a regulator of TH17 cytokines, especially IL-22 production.57,58

In pregnancy, the fetus is similar to an allograft from the perspective of the maternal immune system. Trophoblast invasion from the allogeneic fetus and the shedding of fetal antigens may stimulate a maternal systemic inflammatory response and may therefore cause the emergence of TH17 cells. Contrary to Wegmann's hypothesis, it is surprising that many of the characteristics of a systemic inflammatory response have been demonstrated in normal pregnant women,59 including increased leukocytes,60 monocytic61 and phagocytic activity62 and the production of pro-inflammatory cytokines, such as IL-6, IL-12, IL-18 and TNF-alpha.63,64 A classical marker of inflammatory activity, C-reactive protein, is increased beginning as early as the fourth week of gestation.65 These phenomena show that pregnancy is a well-controlled systemic inflammatory state. Furthermore, it has been reported that subcellular microparticles that are shed from the placenta are present during normal pregnancy and are increased significantly in PE.66,67 These subcellular microparticles shed from the placenta are pro-inflammatory and can stimulate peripheral blood mononuclear cells in healthy non-pregnant females to produce TNF-alpha, IL-12, IL-18 and IFNG. Therefore, such microparticles might contribute to the maternal systemic inflammation observed in both normal and pre-eclamptic pregnancies.68 In addition, the microparticles, cellular debris and exosomes shed by the allogeneic fetus can be captured by antigen-presenting cells, contribute to the priming of fetal-reactive T cells during pregnancy.69 However, whether these fetal antigens have a direct relationship with the differentiation of TH17 has not yet been resolved.

We and others have observed low numbers of TH17 cells and low levels of the TH17-related mRNAs RORC and IL-23R in the deciduas during normal human pregnancy.25,70 In RSA, increased levels of inflammatory cytokines, including IL-6 and IL-1beta, have been observed, and these cytokines have a positive correlation with the proportion of TH17 cells.12,70 The inflammatory stimulus from local allogeneic fetal antigens, systematic inflammation and increased pro-inflammatory cytokines may induce the differentiation of TH17 cells during pregnancy."

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4220838/

Visitor

I need to correct something. I said: "the receptor is in "every cell in the body".

The article actually says: "The genes for smell receptors are present in almost every cell of the body." It is this I find intriguing.

Visitor

This article ties blood pressure to the microbiome effecting the kidneys. The substance propionate is identified as is acetate. I haven't fit this piece into the puzzle yet, but it is a part. The fact that the receptor is in "every cell in the body" makes it more intriguing. The whole piece is good.

How Bacteria Help Regulate Blood Pressure

"The researchers have uncovered a direct, molecular-level explanation of how the microbiome conspires with the kidneys and the blood vessels to manipulate the flow of blood.

The smell receptor, called Olfr78, was an orphan at first: It had previously been noticed in the sensory tissues of the nose, but no one knew what specific scent or chemical messenger it responded to. Pluznick began by testing various chemical possibilities and eventually narrowed down the candidates to acetate and propionate. These short-chain fatty acid molecules come from the fermentation breakdown of long chains of carbohydrates — what nutritionists call dietary fiber. Humans, mice, rats and other animals cannot digest fiber, but the bacteria that live in their guts can.

As a result, more than 99 percent of the acetate and propionate that floats through the bloodstream is released by bacteria as they feed. “Any host contribution is really minimal,” Pluznick said. Bacteria are therefore the only meaningful source of what activates Olfr78 — which, further experiments showed, is involved in the regulation of blood pressure.

Our bodies must maintain a delicate balance with blood pressure, as with electricity surging through a wire, where too much means an explosion and too little means a power outage. If blood pressure is too low, an organism loses consciousness; if it’s too high, the strain on the heart and blood vessels can be deadly. Because creatures are constantly flooding their blood with nutrients and chemical signals that alter the balance, the control must be dynamic. One of the ways the body exerts this control is with a hormone called renin, which makes blood vessels narrower when the pressure needs to be kept up. Olfr78, Pluznick and her colleagues discovered, helps drive the production of renin.

How did a smell receptor inherit this job? The genes for smell receptors are present in almost every cell of the body. If in the course of evolution these chemical sensors hooked up to the machinery for manufacturing a hormone rather than to a smell neuron, and if that connection proved useful, evolution would have preserved the arrangement, even in parts of the body as far from the nose as the kidneys are.

Olfr78 wasn’t the end of the story, however. While the team was performing these experiments, they realized that another receptor called Gpr41 was getting signals from the gut microbiome as well. In a paper last year, Pluznick’s first graduate student, Niranjana Natarajan, now a postdoctoral fellow at Harvard University, revealed the role of Gpr41, which she found on the inner walls of blood vessels. Like Olfr78, Gpr41 is known to respond to acetate and propionate — but it lowers blood pressure rather than raising it. Moreover, Gpr41 starts to respond at low levels of acetate and propionate, while Olfr78 kicks in only at higher levels.

Here’s how the pieces fit together: When you — or a mouse, or any other host organism whose organs and microbes talk this way — have a meal and dietary fiber hits the gut, bacteria feed and release their fatty-acid signal. This activates Gpr41, which ratchets down the blood pressure as all the consumed nutrients flood the circulation.

If you keep eating — a slice of pie at Thanksgiving dinner, another helping of mashed potatoes — Gpr41, left to itself, might bring the pressure down to dangerous levels. “We think that is where Olfr78 comes in,” Pluznick said. That receptor, triggered as the next surge of fatty acids arrives, keeps blood pressure from bottoming out by calling for renin to constrict the blood vessels.

The new understanding of how symbiotic bacteria manipulate blood pressure is emblematic of wider progress in linking the microbiome to our vital statistics and health. While vague statements about the microbiome’s effect on health have become commonplace in recent years, the field has moved beyond simply making associations, said Jack Gilbert, a microbiome researcher at the University of Chicago."

https://www.quantamagazine.org/how-bacteria-help-regulate-blood-pressure-20171130/

Visitor

Getting warmer. How is it they so much when suddenly linking it to the mother's microbiome, {been there} like how vaccines could not have any influence. Please.Yet diet becomes a factor and antibiotics can cut both ways.

Autism risk determined by health of mom's gut

"While Lukens' work links the immune system with neurodevelopmental disorders, he emphasized that this in no way suggests that vaccines are contributing to the development of autism. "There's a definite link between the immune response and the developing brain," he said. "It just doesn't have anything to do with vaccines. It's much, much earlier.""

https://www.sciencedaily.com/releases/2018/07/180718113343.htm

Just citing some of my past comments in this thread on the matter.

"It is worth considering that given that many vaccines require a healthy gut microbiome to work effectively, or at all, that the reason gut issues are occurring in some autism and other gut related problems is that it is the bodies attempt to prevent heightened immune response to vaccines, or dietary antigens, or simply a result of an already stimulated immune response, acquired from the mother, to disease pathogens reflecting a deregulated immune system or one hypersensitive."

Posted by: Visitor | January 09, 2016 at 05:32 PM

Visitor

"It may be that vaccines are the main catalyst for the increase in many immune related conditions{fibro, CFS, and others}, but the cumulative vaccine effects are leading to a plethora of effected mothers who are now giving birth to children already headed into autism or more children more susceptible to vaccines themselves leading into autism. So, it is not that vaccines are not an issue in most cases, but that it is getting to where immune changes in mothers response to infection additional vaccines{flu shots} and conditioned immune status effecting infants prenatally too is more often than before enough to bring about autism even before an infant receives their vaccines.

If this is the case, it blurs the line in seeing where the insults take place and ignoring immune effects in mothers by vaccines misses the tie to increased autoimmune and inflammatory diseases in the population at large. Because of these effects a child can now be born with autism beyond the limited "gene only" causes."

Posted by: Visitor | January 09, 2016 at 05:00 PM

Visitor

Genome-wide changes in protein translation efficiency are associated with autism
https://academic.oup.com/gbe/advance-article-pdf/doi/10.1093/gbe/evy146/25135382/evy146.pdf

Supplementary Data

https://oup.silverchair-cdn.com/oup/backfile/Content_public/Journal/gbe/PAP/10.1093_gbe_evy146/1/evy146_supp.zip?Expires=2147483647&Signature=B-gGJWs-SP6sc7XrJe4LyLTWTgVIIB6fT2GRcym3ImKPCXKWtJD-mUdQDwGyYTkW9LeiPYs6QZRD0X63tEli~n2kPtsPIxFiIY8irx45fNH-PT7FQHpdv~EOTulrS-y3TjJMzVVL9kCeAgOO9XS5sRPfOAPJGdeEJbnHF3DuTi67iBBhXqu98PaNvd6hHQhOxWfxTdNHSVvDM98SquP~nMHLsjcmpgmsaVNx7Jh-q9FJtZSU6r8AQVhbbAjpkp8GN87fXY4P1Vj4Zjj9vZPaFu-rr03RtT96CTniDXbOpmR2yBNRdXA0ow1pIEaldUziwLWNZ8HPglThDUN~PJnmUg__&Key-Pair-Id=APKAIE5G5CRDK6RD3PGA

Visitor

https://www.youtube.com/watch?v=RUcaCE6Q2tA

Visitor

Sometimes those who post what you think arte off topic are trying to do a greater good then you have imagined, but thank you for your reply. I admire you, but I have approaches to help that may not be appreciated. I am those with autisms greatest supporters. The pure offensive approach without the intrinsic human appeal is lacking. I have been open including my confusion and pain. We as a community need to trust in this power of appeal to everyone as acknowledges others innate knowledge and desire for goodness to respond to the harm that is occurring. Our fellowman does care..

I realize I am not the best spokesman , but I was dismayed at how quickly AoA censored me when I am among their greatest advocates. Thank you for your response.

John Stone

Hi Visitor,

Sometimes we don’t post comments which seem off-topic.

Best,

John

Visitor

With what I have contributed am I now banned?

Kate C

Dear Visitor, It's terrific to hear Rubenstein's Chopin in the morning. Thanks for that. It's amazing how music calls on different parts of the brain than logical thinking does. I'm wrestling with a Chopin nocturne these days. Sometimes it doesn't work at all, sometimes some of the pieces fall into place. Maybe I can get some of Rubenstein's emotional abandon eventually, but I seem to need to learn the notes before I can let go!

Visitor

https://www.youtube.com/watch?v=YGRO05WcNDk

Visitor

Whatever.
Trying to see things from what is needed for the genetic pool. A woman who could reflect and respond with this degree of biological dysfunction posses something that is of value to the genome. I was arrested by it, so I think I do as well. Exile for the remnant to add to the survival.

Since only Kate seems to get it I will just let the stream of consciousness go a bit and indulge myself since no one will ever believe me.

https://www.youtube.com/watch?v=hL9h2VkEEaY

Hans Litten

Posted by: Visiitor | February 08, 2018 at 02:44 PM

Are you familiar with the website ?

https://epiphanyasd.blogspot.com/

Jenny

Yes, I agree with Kate. I always learn good information from your posts, Visitor. But why such a heavy heart? It is not up to one person to save the world, or the tragically complex puzzle of autism. The outcome of this battle is not resting on your shoulders alone. And when you feel overwhelmed step back, pair down what you know to basics, step away from the screen, go out in the sun,put your feet on the ground, and take a deep breath. People are like rubber bands, we can stretch and stretch, but then we must contract for a while lest we snap. Once out from under the LEDs and fluorescents, find one person to help. They are in need are everywhere, and if you throw one small stone, you will make a ripple, whether you can see the other side of the pond where it might end or not. Go talk to the head of your nearest church, tell him or her how much you know about autism, explain the concept of biomedical solutions, and volunteer to start an exploration and support group for chronic illness. Post your meetings on the church bulletin board or in their weekly newsletter. Build it, they will come. Or maybe contemplate that God or the universe may be showing you that the person you need to help right now, for just a little while, is you. It is critical that people take time for themselves, and that's ok. Have you taken the time to apply the health principals we have all discussed on this site to yourself yet? You can't escape chemistry and physics yourself, you know? Your spirit cannot soar if it is mired in sludge.
How are your D3 levels? Are you eating low carb, higher fat? Have you switched your omega 6's to omega 3s? Are you getting the right and varied probiotics? Checked your B12/folate? Have you discovered topical magnesium? Rid yourself of toxic exposures? Turning off the wireless at night? Surrounding your workspace with sun-mimicking lightbulbs like halogens? Are you "minding your mito?" Grounding yourself while at the computer? Walking in nature periodically to appreciate the beauty that God gave us that still exists in the middle of the chaos. Nobody wants a smart person like you to push themselves to the point of self-sacrifice, that would be self-defeatist in the eyes of any autism-aware person.

Visiitor

Kate C,

I don't understand why I could not have become involved with someone like you, instead in what I was arrested by in my focus. That is a scientific statement, not a social one.

Visitor

Kate C ,

To know that even one is so aware of these matters bolsters my spirit. I don't know if I can persist in searching for answers, but you give me hope. To infinity and beyond. Thank you for your kindness.

Visitor

Kate C

Dear Visitor, I have always read and reread your posts. I value them because they are science-driven, compassionate approaches to finding the causes of autism. I hope that having gone "off the rails" refers to the period of time between your postings, and not to any feelings of inadequacy. Because from where I stand, you are incredibly competent and intelligent. Your postings give me hope. Please don't stop.

Visitor

To anyone. I apologize that I have gone off the rails. I don't know if anything I have posted has ever made any difference, but I tried with every fiber my being to bring light to these matters. I have so much love and respect for almost all who post on AoA. I have found I am all too human and don't know if I am objective. The immensity of all this and my own personal experience makes discerning reality a fulltime challenge and more often I am thinking I cannot ever catchup. God bless Dr. Wakefield who has a character and insight that is pure blessing and defies description. I admire him from afar.

" Assembly-line medicine kills doctors. Brilliant, compassionate people can't care for complex patients in 15-minute slots. When punished or fired by administrators for "inefficiency" or "low productivity," doctors may become suicidal. Pressure from insurance companies and government mandates crush these talented people who just want to help patients. Many doctors cite inhumane working conditions in their suicide notes."

Visitor

A lot of us have known about LPS, bacteria, and candida problems in autism forever, but trying to piece all the elements and processes into a complete picture from start to finish and understand the minute details of the processes makes for many recapitulations as though it is new, at least for me, when it is actually some stuff that was found and noted at the outset. I noticed a doctor's video on another thread about candida and there was a lot of truth in it. One of the first things we did was deal with the gut dysbiosis and candida. The constant dismissal over years made me think I had to continue to prove these aspects.

From many years back.
Gut Microorganisms and Autism: the Latest Research 1999 Sep 26-29
http://www.microbialinfluence.com/candida.html

Visitor

Jenny,
MIR-155 is a master inflammation regulator and as you say, is involved in many conditions. Ones that I have peaked my interest are H. Pylori control, arthritis, migraines, Diabetes, obesity, MS, Down syndrome, lupus, and of course autism. There is clearly a different amount of function in different conditions and the amounts in relation to foxp3, MIF, brain function and BBB integrity are on one side, but skin and gut function aspects of mir-155 seem to be out of sync, for lack of a better description at this point. Here are s a few info bits on it. Impaired signaling and development in T and B cells is a part of the issue it appears.

miR-155: an ancient regulator of the immune system

Summary

"MicroRNAs (miRNAs) are a newly recognized class of regulatory genes which repress the expression of protein-coding genes. Numerous studies have uncovered a complex role for miRNAs regulating many aspects of a variety of cellular processes including cell growth, differentiation, and lineage commitment. In the immune system, miR-155 is unique in its ability to shape the transcriptome of activated myeloid and lymphoid cells controlling diverse biological functions ranging from inflammation to immunological memory. Not surprisingly, a tight control of miR-155 expression is required to avoid malignant transformation, as evidenced by miR-155 overexpression in many cancers of B-cell origin. In this review, we discuss the potential of miR-155 as a molecular target for therapeutic intervention and discuss the function of miR-155 in the context of protective immunity. We first look back into the emergence of miR-155 in evolution, which is coincidental with the emergence of the ancestors of the antigen receptors. We then summarize what we have learned about the role of miR-155 in the regulation of lymphoid subsets at the cellular and molecular level in the context of recent progress in this field."

http://onlinelibrary.wiley.com/doi/10.1111/imr.12057/full

Requirement of bic/microRNA-155 for Normal Immune Function

Abstract

"MicroRNAs are a class of small RNAs that are increasingly being recognized as important regulators of gene expression. Although hundreds of microRNAs are present in the mammalian genome, genetic studies addressing their physiological roles are at an early stage. We have shown that mice deficient for bic/microRNA-155 are immunodeficient and display increased lung airway remodeling. We demonstrate a requirement of bic/microRNA-155 for the function of B and T lymphocytes and dendritic cells. Transcriptome analysis of bic/microRNA-155–deficient CD4+ T cells identified a wide spectrum of microRNA-155–regulated genes, including cytokines, chemokines, and transcription factors. Our work suggests that bic/microRNA-155 plays a key role in the homeostasis and function of the immune system."

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2610435/

MicroRNA-155 is essential for the T cell-mediated control of Helicobacter pylori infection and for the induction of chronic Gastritis and Colitis.

Abstract

"MicroRNAs govern immune responses to infectious agents, allergens, and autoantigens and function by posttranscriptional repression of their target genes. In this paper, we have addressed the role of microRNA-155 (miR-155) in the control of Helicobacter pylori infection of the gastrointestinal tract and the development of H. pylori-induced chronic gastritis and associated gastric preneoplastic pathology. We show that miR-155 is upregulated in the gastric mucosa of experimentally infected mice and that miR-155(-/-) mice fail to control H. pylori infection as a result of impaired pathogen-specific Th1 and Th17 responses. miR-155(-/-) mice are also less well protected against challenge infection after H. pylori-specific vaccination than their wild-type (wt) counterparts. As a consequence of their impaired T cell responses to H. pylori, miR-155(-/-) mice develop less severe infection-induced immunopathology manifesting as chronic atrophic gastritis, epithelial hyperplasia, and intestinal metaplasia. T cells from miR-155(-/-) mice that are activated by CD3/CD28 cross-linking expand less and produce less IFN-γ and IL-17 than wt T cells. Finally, we show in this paper using adoptive transfers that the phenotypes of miR-155(-/-) mice are likely due to T cell-intrinsic defects. In contrast to wt T cells, miR-155(-/-) T cells from infected donors do not control H. pylori infections in T cell-deficient recipients, do not differentiate into Th1 or Th17 cells, and do not cause immunopathology. In addition, naive miR-155(-/-) T cells fail to induce chronic Th17-driven colitis in an adoptive transfer model. In conclusion, miR-155 expression is required for the Th17/Th1 differentiation that underlies immunity to H. pylori infection on the one hand and infection-associated immunopathology on the other."

https://www.ncbi.nlm.nih.gov/pubmed/21880981

Helicobacter pylori Induces miR-155 in T Cells in a cAMP-Foxp3-Dependent Manner

Abstract

"Amongst the most severe clinical outcomes of life-long infections with Helicobacter pylori is the development of peptic ulcers and gastric adenocarcinoma - diseases often associated with an increase of regulatory T cells. Understanding H. pylori-driven regulation of T cells is therefore of crucial clinical importance. Several studies have defined mammalian microRNAs as key regulators of the immune system and of carcinogenic processes. Hence, we aimed here to identify H. pylori-regulated miRNAs, mainly in human T cells. MicroRNA profiling of non-infected and infected human T cells revealed H. pylori infection triggers miR-155 expression in vitro and in vivo. By using single and double H. pylori mutants and the corresponding purified enzymes, the bacterial vacuolating toxin A (VacA) and γ-glutamyl transpeptidase (GGT) plus lipopolysaccharide (LPS) tested positive for their ability to regulate miR-155 and Foxp3 expression in human lymphocytes; the latter being considered as the master regulator and marker of regulatory T cells. RNAi-mediated knockdown (KD) of the Foxp3 transcription factor in T cells abolished miR-155 expression. Using adenylate cyclase inhibitors, the miR-155 induction cascade was shown to be dependent on the second messenger cyclic adenosine monophosphate (cAMP). Furthermore, we found that miR-155 directly targets the protein kinase A inhibitor α (PKIα) mRNA in its 3′UTR, indicative of a positive feedback mechanism on the cAMP pathway. Taken together, our study describes, in the context of an H. pylori infection, a direct link between Foxp3 and miR-155 in human T cells and highlights the significance of cAMP in this miR-155 induction cascade."

http://journals.plos.org/plosone/article?id=10.1371/journal.pone.0009500

The microRNA miR-155 controls CD8+ T cell responses by regulating interferon signaling

http://www.nature.com/articles/ni.2576?error=cookies_not_supported&code=09228270-cc3f-4dca-b9bf-733dc74e9053

microRNA-155 Regulates the Generation of Immunoglobulin Class-Switched Plasma Cells

http://www.sciencedirect.com/science/article/pii/S1074761307005031

Expression of miRNA 155, FOXP3 and ROR gamma, in children with moderate and severe atopic dermatitis.

Abstract

BACKGROUND:

"Atopic dermatitis is a disease characterized by a chronic inflammatory process in the skin, but its link to miRNA 155 is less known. The aim of the study was to evaluate the expression of microRNA155, and T helper type 17 cells and Treg cells in children with atopic dermatitis.

METHODS:

The study population consisted of: children seen for atopic dermatitis at the outpatient ambulatory of Dermatology at the Children Hospital Regina Margherita, Torino, Italy,( n = 23); healthy control subjects ( n =23). Blood samples were taken during routine control analysis and the expression of miRNA 155 and the production of FOXP3 and RORˠ was determined using PCR real time.

RESULTS:

The analysis of miR-155 shows that the over-expression of miR-155 is statistically significant (p = 0.0040) in the group of patients with atopic dermatitis compared to the healthy control group. Analysis of mRNAs of FOXP3 and RORˠ shows a FOXP3 mRNA expression statistically higher in the group of patients (p = 0.0057). The Th17 / Treg ratio is significantly smaller in patients with atopic dermatitis (p = 0.0012). Also the ratio miR-155/Th17/Treg is larger in the group of patients with atopic dermatitis (p = 0.0002).

CONCLUSIONS:

Our results suggest that increased miR-155 and FOXP3 and RORˠ responses may provide a link to immune dysregulation associated with atopic dermatitis. Although a point-by-point correlation between miR-155 and the ratio Th17/Treg is not demonstrated, our findings shows that these two elements do not appear to be completely unrelated to each other."

https://www.ncbi.nlm.nih.gov/pubmed/29249119

Cutting edge: the Foxp3 target miR-155 contributes to the development of regulatory T cells.

Abstract

"Foxp3 is a transcription factor that is essential for the normal development of regulatory T cells (Tregs). In the absence of microRNAs (miRNAs), Foxp3(+) Tregs develop but fail to maintain immune homeostasis, leading to a scurfy-like disease. Global analysis of the network of genes regulated by Foxp3 has identified the miRNA miR-155, which is highly expressed in Tregs, as a direct target of Foxp3. In this study we report that miR-155-deficient mice have reduced numbers of Tregs, both in the thymus and periphery, due to impaired development. However, we found no evidence for defective suppressor activity of miR-155-deficient Tregs, either in vitro or in vivo. Our results indicate that miR-155 contributes to Treg development, but that additional miRNAs control Treg function."

https://www.ncbi.nlm.nih.gov/pubmed/19234151

The role of miR-155 in regulatory T cells and rheumatoid arthritis

http://www.sciencedirect.com/science/article/pii/S1521661613000831

MicroRNA-155 Promotes Autoimmune Inflammation by Enhancing Inflammatory T Cell Development

http://www.sciencedirect.com/science/article/pii/S1074761310003511

This last one makes me think impaired IL-17 in the gut may allow for Candida increases.

Impaired IL-17 Production in Gut- Residing Immune Cells of 5xFAD Mice with Alzheimer's Disease Pathology.

Abstract

"Alzheimer's disease (AD) is characterized by accumulation of amyloid-β plaques that further promotes microglia-mediated neuroinflammatory responses and inflammation in the brain. Emerging data are revealing the relation between gut-associated lymphoid tissue (GALT) cells and CNS, as effector cells primed in the gut might home to the brain. This study aimed to determine cell composition of GALT in 5xFAD mice, an established model for AD. Immune cells isolated from Peyer's patches (PP) and mesenteric lymph nodes (MLN) were stained with surface and intracellular markers for T helper (Th) subpopulations, B lymphocytes and macrophages and analyzed cytofluorimetrically, while cytokine expression and production were determined by qPCR and ELISA, respectively. Inflammation was detected in GALT of 5xFAD mice with established AD pathology. Although the production of IFN-γ, IL-4, and IL-10 was comparable between the strains, lower IL-17 production was observed in PP and MLN cells. This phenomenon could not be attributed to a lower abundance of Th17 cells, or cytokines that initiate their formation or propagation (TGF-β, IL-6, and IL-23). Also, reduced IL-17 production was not a consequence of altered Il-17 mRNA transcription or deficiency of Rorγt, a key transcription factor for IL-17. However, the expression of miR-155 (a non-coding micro RNA that promotes the development of Th17 cells), was significantly lower in MLN cells of 5xFAD mice. In contrast, mice without AD neuropathology did not have inflammation in GALT or altered Th17 numbers, nor decreased IL-17 production. In conclusion, the observed changes in GALT of 5xFAD mice mirror the disease progression and might reflect inadequate immune surveillance in the gut and lead to enhanced AD pathology."

https://www.ncbi.nlm.nih.gov/pubmed/29254086

Jenny

The mir55 info is very interesting, sitting at the juncture of all these chronic diseases which seem to keep intersecting each other.

Visitor

This is likely involved in our case and degrees of it in others, but having discussed hyperemesis gravidarum in the past here and having long seen Helicobacter pylori as playing a role I had found this interesting. The second report one is notable too. If you have read the recent report on Natural Killer cells function in uterine fetus development the third report may show connections with the last report on Heme Oxygenase and it's impact on immune cells NK cells, T c& B cells.. {may be tying into Jaundice, biliverdin, bilirubin} The uterine NK cells also deal with the uterine lining to remove inflammation and also deal with pathogens. like bacteria.

Helicobacter pylori and pregnancy-related disorders

"Abstract

"Helicobacter pylori (H. pylori) infection is investigated in gastric diseases even during pregnancy. In particular, this Gram-negative bacterium seems to be associated with hyperemesis gravidarum, a severe form of nausea and vomiting during pregnancy. During the last decade, the relationship among H. pylori and several extra-gastric diseases strongly emerged in literature. The correlation among H. pylori infection and pregnancy-related disorders was mainly focused on iron deficiency anemia, thrombocytopenia, fetal malformations, miscarriage, pre-eclampsia and fetal growth restriction. H. pylori infection may have a role in the pathogenesis of various pregnancy-related disorders through different mechanisms: depletion of micronutrients (iron and vitamin B12) in maternal anemia and fetal neural tube defects; local or systemic induction of pro-inflammatory cytokines release and oxidative stress in gastrointestinal disorders and pre-eclampsia; cross-reaction between specific anti-H. pylori antibodies and antigens localized in placental tissue and endothelial cells (pre-eclampsia, fetal growth restriction, miscarriage). Since H. pylori infection is most likely acquired before pregnancy, it is widely believed that hormonal and immunological changes occurring during pregnancy could activate latent H. pylori with a negative impact not only on maternal health (nutritional deficiency, organ injury, death), but also on the fetus (insufficient growth, malformation, death) and sometime consequences can be observed later in life. Another important issue addressed by investigators was to determine whether it is possible to transmit H. pylori infection from mother to child and whether maternal anti-H. pylori antibodies could prevent infant’s infection. Studies on novel diagnostic and therapeutic methods for H. pylori are no less important, since these are particularly sensitive topics in pregnancy conditions. It could be interesting to study the possible correlation between H. pylori infection and other pregnancy-related diseases of unknown etiology, such as gestational diabetes mellitus, obstetric cholestasis and spontaneous preterm delivery. Since H. pylori infection is treatable, the demonstration of its causative role in pregnancy-related disorders will have important social-economic implications."

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3921475/

The choroid plexus epithelium as a novel player in the stomach-brain axis during Helicobacter infection.

Abstract

"Several studies suggest a link between shifts in gut microbiota and neurological disorders. Recently, we reported a high prevalence of Helicobacter suis (H. suis) in patients with Parkinson's disease. Here, we evaluated the effect of gastric H. suis infection on the brain in mice. One month of infection with H. suis resulted in increased brain inflammation, reflected in activation of microglia and cognitive decline. Additionally, we detected choroid plexus inflammation and disruption of the epithelial blood-cerebrospinal fluid (CSF) barrier upon H. suis infection, while the endothelial blood-brain barrier (BBB) remained functional. These changes were accompanied by leakage of the gastrointestinal barrier and low-grade systemic inflammation, suggesting that H. suis-evoked gastrointestinal permeability and subsequent peripheral inflammation induces changes in brain homeostasis via changes in blood-CSF barrier integrity. In conclusion, this study shows for the first time that H. suis infection induces inflammation in the brain associated with cognitive decline and that the choroid plexus is a novel player in the stomach-brain axis."

https://www.ncbi.nlm.nih.gov/pubmed/29258921

This next one is quite good. While posting only the abstract I suggest reading it all.

Effects of heme oxygenase-1 on innate and adaptive immune responses promoting pregnancy success and allograft tolerance

"The heme-degrading enzyme heme oxygenase-1 (HO-1) has cytoprotective, antioxidant, and anti-inflammatory properties. Moreover, HO-1 is reportedly involved in suppressing destructive immune responses associated with inflammation, autoimmune diseases, and allograft rejection. During pregnancy, maternal tolerance to foreign fetal antigens is a prerequisite for successful embryo implantation and fetal development. Here, HO-1 has been implicated in counteracting the overwhelming inflammatory immune responses towards fetal allo-antigens, thereby contributing to fetal acceptance. Accordingly, HO-1 ablation negatively impacts the critical steps of pregnancy such as fertilization, implantation, placentation, and fetal growth. In the present review, we summarize recent data on the immune modulatory capacity of HO-1 towards allo-antigens expressed by the semi-allogeneic fetus and organ allografts. In this regard, HO-1 has been shown to promote alloantigen tolerance by blocking dendritic cell maturation resulting in reduced T cell responses and increased numbers of regulatory T cells. Moreover, HO-1 is suggested to shift the uterine cytokine milieu towards a protective Th2 profile and protects fetal tissue from apoptosis by upregulating anti-apoptotic molecules. Thus, HO-1 is not only a pivotal regulator of the initial steps of pregnancy; but also, an important player in supporting the maternal immune system in tolerating the fetus.

https://www.frontiersin.org/articles/10.3389/fphar.2014.00288/full

Looking at mir-155 effecting Osteoglycin. Osteoglycin is mentioned as being produced by NK cells in this last piece.

The body’s killer immune cells also feed fetuses in the womb

"The immune system’s aggressive natural killer cells – which normally kill cancer cells and infectious pathogens – also help nourish early fetuses, helping them grow.

This discovery was made by Zhigang Tian of the University of Science and Technology of China, in Hefei, and his team. Analysing natural killer cells from mice, they identified a subset that’s only produced in the uterus, and only during early pregnancy.

They named these “uterine NK cells”, and found that these cells produce large quantities of two proteins that are vital for growing fetuses.

One of these proteins, called pleiotrophin, drives the growth of blood vessels, bone, cartilage and brain fibres. The other protein, osteoglycin, orchestrates heart development and healthy growth of skin and eyes.

When the researchers examined womb tissue from 54 women, they found that those who had recently experienced miscarriages had fewer uterine NK cells than those who’d had successful pregnancies."

https://www.newscientist.com/article/2157018-the-bodys-killer-immune-cells-also-feed-fetuses-in-the-womb/

Visitor

greyone

Close to 10 years ago I had researched that idea and ended up doing a protocol designed to handle intracellular pathogens. My wife was on Olmesartan for well over 4 years. The vitamin D issue is certainly not settled though pro D is ascendant. The Olmesartan does a lot more than activate the VDTR, it also blocks the AT1 receptor raises SOD and controls TNF-A and other cytokines.
Have posted about Autophagy a few times over the last few years in this thread.
Here is from 2013 I

nflammaging: disturbed interplay between autophagy and inflammasomes

http://www.impactaging.com/papers/v4/n3/full/100444.html
Hve been down the MTOR path too for a good while, but the you tube speaker is on target as far as I have listened to him.

greyone

"Some authorities now believe that low 25(OH)D is a consequence of chronic inflammation rather than the cause. Research points to a bacterial etiology pathogenesis for an inflammatory disease process which results in high 1,25(OH)2D and low 25(OH)D. Immunotherapy, directed at eradicating persistent intracellular pathogens, corrects dysregulated vitamin D metabolism and resolves inflammatory symptoms."
(interesting flow chart illustrations to the study)
https://www.ncbi.nlm.nih.gov/pubmed/25048990


autophagy cure or curse, a lecture by Dr Steven Phillips, focused on neurodegenerative disease
https://youtu.be/5_EiB_yCA7U

Visitor

Benedetta,
You are correct about TB and Lipopolysaccharide. I had read that it did not have it on the outer wall when dormant. This aspect is new to me and I am trying to understand how LPS levels are raised in people with the levels attributed to a dormant bacteria. I had read; " nonreplicating cells do not synthesize new cell wall" in reference to TB. I did not make that clear at all.

I put the wrong substance in that last post too. It is Lipoarabinomannan, that is a component of the TB cell wall that elicits inflammation or heightens it. Either way, TB, mycoplasma, and Helicobacter pylori are infections that have been in my scope along with Strep. I had generally though at least a part of the lipopolysaccharide was coming through the leaky gut, but pathogens also in the rest of the system added to the mix.

Increased circulatory levels of lipopolysaccharide (LPS) and zonulin signify novel biomarkers of proinflammation in patients with type 2 diabetes.

https://www.ncbi.nlm.nih.gov/pubmed/24347174

Low serum vitamin D levels in type 2 diabetes patients are associated with decreased mycobacterial activity.

https://www.ncbi.nlm.nih.gov/pubmed/28882103

This is an outside possibility of involvement.

TLR4-NOX2 axis regulates the phagocytosis and killing of Mycobacterium tuberculosis by macrophages.

https://www.ncbi.nlm.nih.gov/pubmed/29233104

Implication of Cytotoxic Helicobacter pylori Infection in Autoimmune Diabetes

https://www.hindawi.com/journals/jdr/2016/7347065/

Helicobacter pylori CagA antibodies and thyroid function in latent autoimmune diabetes in adults

http://www.europeanreview.org/article/11526

and this that is just interesting...

Helicobacter pylori Infection and Graft-versus-Host Disease

https://www.sciencedirect.com/science/article/pii/S1083879110005136

{Autophagy has been connected to Autism}

Innate immunity to mycobacteria: vitamin D and autophagy.

Abstract

"Autophagy is an ancient mechanism of protein degradation and a novel antimicrobial strategy. With respect to host defences against mycobacteria, autophagy plays a crucial role in antimycobacterial resistance, and contributes to immune surveillance of intracellular pathogens and vaccine efficacy. Vitamin D3 contributes to host immune responses against Mycobacterium tuberculosis through LL-37/hCAP-18, which is the only cathelicidin identified to date in humans. In this review, we discuss recent advances in our understanding of host immune strategies against mycobacteria, including vitamin D-mediated innate immunity and autophagy activation. This review also addresses our current understanding regarding the autophagy connection to principal innate machinery, such as ubiquitin- or inflammasome-involved pathways. Integrated dialog between autophagy and innate immunity may contribute to adequate host immune defences against mycobacterial infection."

https://www.ncbi.nlm.nih.gov/pubmed/20557314

greyone

visitor
so perhaps its not specifically the latency, as much as, or in addition to ability of some bacteria to subvert autophagy (remove abnormal proteins) eg bartonella, brucellosis and coxiella (borreliosis unknown).

Benedetta

I am not sure what you mean by production of lipopolysaccharide, but TB is like all gram negative bacteria, and lipopolysaccharide is very much present as the outer coat of that bacteria too?

TB or TB like bacteria does seems to keep showing up both in literature and in our own back yards. .

I thought TB was very much taken care of and not so much because of antibiotics, but by pasteurizing the milk.

Even with antibiotics - what happens is that the TB bacteria is never gotten rid of. The patient that is considered cured, still has it. The antibiotic just helped the patient's body to encapsulate or encase the bacteria. So a person that once had TB still has an encapsulated bacteria still within their lungs.

This fall there has been a huge number of deer dying in the woods from a wasting disease from a bacteria some what like TB, if not TB. Some times I do wonder if they really can figure out different variants of microbes, or even able to figure out what they can morph into.

This was in Kentucky. IT was so bad that the woods, waffled with the stench of rotting meat. This was here in Kentucky. But my child hood friend up in Michigan said it was the same thing gong on up there. That one farmer with a large farm had around 80 head of cattle come down with it, and the deer around his farm had it too.

We our own selves had four cows die of a wasting disease; even though the vet said old age. Hmmmm, don't think I believe that? Some of our cattle showed lameness in the back hips, then loss of weight. All regain their vigor and strength during the summer and although I agree that they were old ; they still were having calves. However; one of the younger cows were salivating extensively this spring and even though she is okay now, I think she is still on the thin side. I don't think she is going to have a calf this year, she does not look like it.

There was a cycle going on, that involve midges, water borne sucking little insects.

We ran over two baby deer this summer in our hay field. Twins, I felt really bad about it, but it was an accident and could not be helped. However it shows you just how there is contact between cattle, deer, water, food out there. Cattle of course we are closely linked to also.

There was a very well written article - I forgot the author and such, but it can be found on the internet that the prions they found in the brains of the victims of mad cow disease were really remnants of the TB bacteria. It may be that there are no such thing as prions, that is still just a theory. I have looked at it and I do know that in Organic Chemistry there was left and right molecules and it could throw a wrench some of the chemical reactions - I just don't see how they can make more of themselves? How can proteins take on what we consider the definition of life and can reproduce; make more of themselves? It makes more sense that Prions instead may be more of a signs of a slow growing; few and far between, very missed pathogenic bacteria.

And what does it take to kill these stealthy bacteria if that is true.
There was an article a while back that was sounding the alarm that the deep brain probes they were using on patients that turned out to have some kind of form of mad cow disease - were spreading to other patients that did not . Even though they were cleaning the probes between procedures apparently what they thought was disinfecting the probes was not enough to kill the prions- proteins with molecules turned the wrong way. Perhaps it was not enough to kill a few undetected bacteria.


Visitor

For other reasons I had felt it could not be TB and while TB does evoke lipopolysaccharide-binding protein and bind to it TB does not produce lipopolysaccharide which is stated to be elevated in those with the bacteria.

Visitor

greyone

I would believe so, given their persistence and dormancy, but many types of bacteria can become dormant. It does not speak of spores or allude to pleomorphic bacteria, so that is a mystery. It surely isn't tb, but tb fits somewhat as it is very slow growing and can become latent and tb has some connections with diabetes.. I don't know why the full report did not say anything more about the bacteria as they seem to imply they have isolated it. Either it is an unknown type or they want to keep the information to themselves at this point. I thought it interesting they mention leaky gut as that is how we see some problems coming about and I have been curious about such a pathogen for a long time.

Here is one quote. from the paper linked below.

""T2D is accompanied by long-term inflammation, and this inflammation is mediated in part by increased fibrinogen levels, as well as a changed cytokine profile that is driven, at least in part, by dysregulated glucose and insulin function. The origin of this inflammation is mostly unclear and remains unresolved in diabetes. It is known that gut dysbioses and atopobioses71 (colloquially referred to as ‘leaky gut’) are a well-known contributor to the pathogenesis of many metabolic diseases, including obesity146, T1D147, 148, T2D146, 149, 150, and CVD151. We have previously suggested that there is a fundamental link between gut dysbioses, the presence of a (dormant) blood microbiome and the presence of the highly inflammatory LPS71""

Lipopolysaccharide-binding protein (LBP) reverses the amyloid state of fibrin seen in plasma of type 2 diabetics with cardiovascular co-morbidities

http://www.nature.com/articles/s41598-017-09860-4

greyone

visitor
saw your post about Pretorius and Kell.
does this point toward the slower dividing bacteria, longer latencies?

Verify your Comment

Previewing your Comment

This is only a preview. Your comment has not yet been posted.

Working...
Your comment could not be posted. Error type:
Your comment has been saved. Comments are moderated and will not appear until approved by the author. Post another comment

The letters and numbers you entered did not match the image. Please try again.

As a final step before posting your comment, enter the letters and numbers you see in the image below. This prevents automated programs from posting comments.

Having trouble reading this image? View an alternate.

Working...

Post a comment

Comments are moderated, and will not appear until the author has approved them.

Your Information

(Name and email address are required. Email address will not be displayed with the comment.)