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» LymeNet Flash » Questions and Discussion » Medical Questions » Recalibrate 'fight or flight' - HPA Axis Dysfunction trick

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Author Topic: Recalibrate 'fight or flight' - HPA Axis Dysfunction trick
kday
LymeNet Contributor
Member # 22234

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"Akin to pulling back a slingshot, temporarily reducing the bioavailability of cortisol pharmacologically causes the HPA axis to overcompensate and launch itself back into a correct regulatory regime."

http://www.prohealth.com/library/showarticle.cfm?libid=14271

-------

"Inhibitors of cortisol synthesis include pharmaceutical agents such as ketoconazole that have been used in limited human trials."

Ketoconazole is an anti-fungal.

"A number of chronic diseases have been characterized by abnormalities in HPA axis regulation. These include major depression and its subtypes, anxiety disorders such as post-traumatic stress disorder, panic disorder and cognitive disorders such as Alzheimer's disease and minimal cognitive impairment of aging. Dysregulation of the HPA axis has also been linked to the pathophysiology of Gulf War illness, post-infective fatigue, and chronic fatigue syndrome (CFS)."

If you like technical stuff, it can be found in this journal:

http://www.ploscompbiol.org/article/info%3Adoi%2F10.1371%2Fjournal.pcbi.1000273

Posts: 967 | From A deserted island without internet access | Registered: Sep 2009  |  IP: Logged | Report this post to a Moderator
dali
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Member # 24458

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Thank you k-day. I also read your blog...keep it up!
I do believe that this infection can cause major dysregulation of gland and organ systems, and that balancing these is key to maintaining functionality during the "curative" (antibiotic) phase.
have a good day!

Posts: 172 | From ohio | Registered: Feb 2010  |  IP: Logged | Report this post to a Moderator
Carol in PA
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kday,
I googled this med after I read your post.

It's also used for Cushing's Syndrome, an endocrine disorder.
It can be purchased as a pet medication, Nizoral.

Diflucan is an anti-fungal medication in the same family of drugs as Nizoral.
I've read that there is a Lyme protocol from Dr. Schardt in Germany that uses Diflucan.

Maybe the reason that it's effective is because it helps to fix the HPA axis.

Where's Marnie?

Carol

Posts: 6947 | From Lancaster, PA | Registered: Feb 2004  |  IP: Logged | Report this post to a Moderator
cantgiveupyet
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maybe this is why I feel better when i take Ketoconazole

just a warning watch liver function - after i was on it 6 months - it raised my levels.

--------------------
"Say it straight simple and with a smile."

"Thus the task is, not so much to see what no one has seen yet,
But to think what nobody has thought yet, About what everybody sees."

-Schopenhauer

pos babs, bart, igenex WB igm/igg

Posts: 3156 | From Lyme limbo | Registered: Oct 2005  |  IP: Logged | Report this post to a Moderator
Lymeorsomething
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It's an interesting concept, but the study doesn't really lay forth a clear protocol to follow.

It seems like you would have to nail certain target thresholds (certain ACTH rebound, etc.) in order to make the thing work.

--------------------
"Whatever can go wrong will go wrong."

Posts: 2062 | From CT | Registered: Jul 2008  |  IP: Logged | Report this post to a Moderator
Marnie
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Might want to warn your friends and spouse first because:

"Low levels of salivary cortisol associated with aggressive behavior"

Bb applied the brakes to our immune system from the get-go. You already have many low cortisol symptoms.

This is the beginning of Bb's mischief with regards to our immune reaction to his invasion:

Salp 15 protein in the tick's saliva binds to Bb's OspC and inhibits Th2 (allergic reaction).

Though PGE2 may try to kick it in.

"Prostaglandin E2 does enhance
production of Th2 cytokines and down regulate Th1
cytokines and inhibit T-lymphocyte proliferation

Salivary prostaglandin E2 and I2 are vasodilators
and inhibitors of platelet aggregation.

Tick saliva often contains high concentrations of prostaglandins. Prostaglandin E2
(PGE2) occurs in the salivary glands of Boophilus
microplus,

***I. scapularis*** and..."

Anti Salp 15 proteins have helped (!):

"At 3 weeks, when spirochetes have disseminated to diverse organs, the pathogen burden in the heart and joints was also significantly lower in mice given Salp15-antiserum."

And apparently giving Salp 15 proteins BEFORE Bb was present and could cloak itself in it ->

"mice given four infestations

with pathogen free I. scapularis nymphs

were resistant to B. burgdorferi transmission by a subsequent infestation with infected nymphs."

As long as Bb is not present in the tick's saliva, the saliva components alone, picked up by the young ticks and transmitted into the mice looked to trigger an immunity. Like getting a vaccine before being exposed to a disease!

The tick's saliva contains a lot of things that drive down our response and allow Bb to thrive.

First Bb infects the epithelial cells that line the blood vessels. Along comes the DC cells which are like roving policemen who are supposed to "capture" Bb and take him away. Along the way to "jail", the DC cells are supposed to begin the destruction process so when Bb goes before the "judge", his real self is obvious, but the DC cells get infected themselves and Bb robs THEM of glucose too. He wounds the police persons who have arrested him.

That was my attempt to put the following in "English":


We here demonstrate, to our knowledge for the first time, that the Ixodes scapularis salivary protein Salp15 inhibits adaptive immune responses by

suppressing human dendritic cell (DC) functions.

Salp15 inhibits both Toll-like receptor- and B. burgdorferi-induced production of pro-inflammatory cytokines by DCs and DC-induced T cell activation.

Salp15 interacts with DC-SIGN on DCs, which results in activation of the serine/threonine kinase Raf-1.

Strikingly, Raf-1 activation by Salp15 leads to mitogen-activated protein kinase kinase (MEK)-dependent decrease of IL-6 and TNF-α mRNA stability and impaired nucleosome remodeling at the IL-12p35 promoter.

These data demonstrate that Salp15 binding to DC-SIGN triggers a novel Raf-1/MEK-dependent signaling pathway acting at both cytokine transcriptional and post-transcriptional level to modulate Toll-like receptor-induced DC activation, which might be instrumental to tick feeding and B. burgdorferi infection, and an important factor in the pathogenesis of Lyme disease.

DC-SIGN (Dendritic Cell-Specific Intercellular adhesion molecule-3-Grabbing Non-integrin) is also known as CD209.

It is on DC cells and macrophages. It is an adhesion molecule.

In another pathogen very similar thing happens:

We and others recently demonstrated that the C type lectins L-SIGN and *DC-SIGN* capture hepatitis C virus (HCV) by specific binding to

envelope glycoprotein E2.

Cellular binding of hepatitis C virus envelope glycoprotein E2 requires cell surface heparan sulfate...

The binding is supposed to activate phagocytosis. (Sorta a "gobble them up")

Doesn't happen. Our macrophages (think of them as pac men) don't work.

Because of this:

Utilization of N-acetylglucosamine
polymers

or chitin (available in the arthropod
host) as a substrate for cell wall biosynthesis

(glucosamine deacetylase, NagA; BB0151) and/or as an energy source (glucosamine deaminase, NagB; BB0152) could represent an adaptation
of B. burgdorferi for survival in its specific niche, in this case the arthropod host.

If Bb has NagA and/or NagB there goes N-acetylglucosamine which is needed for the vitamin D precursor binding protein (Gc) to activate MAF (macrophage activating factor).

So...Bb robs a carbohydrate off a glycoprotein that is needed to make the vitamin D binding protein in order to activate our pac men.

Consequently, the macrophages can't work and like all the other infected defense cells, they are headed for cell death.

Now for some "hope for a cure".

A *Salmonella* enterica serovar Typhimurium aroA-deficient delivery system was used to

*target the immunosuppressive protein Salp15 to antigen-presenting cells*

In vitro and in vivo infections

with Salp15-containing Salmonella

resulted in an impaired CD4+-T-cell activation, suggesting that the protein was produced by antigen-presenting cells in a physiologically active form.

Now read this research:

http://www.sciencedaily.com/releases/2008/02/080229171124.htm

Title: Salmonella Bacteria Turned Into Cancer Fighting Robots

Or this...note the date at the top:

http://www.deccanchronicle.com/health/salmonella-bugs-can-help-fight-cancer-217

Meanwhile, GcMAF will hopefully get off the ground as a treatment. It is LOGICAL.

Or somebody will realize that substituting a ketone to rev up the infected glucose starved defense cells might work too.

ICHT = ATP
Photon therapy = ATP
Axona medicinal food = ATP

GcMAF...help out the macrophages.

Those support our own infected defense cells.

But going after Bb via ALTERED Salmonella might work someday too.

Keep the faith.

Posts: 9424 | From Sunshine State | Registered: Mar 2001  |  IP: Logged | Report this post to a Moderator
   

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