posted
"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."
"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:
posted
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
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Carol in PA
Frequent Contributor (5K+ posts)
Member # 5338
posted
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
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cantgiveupyet
Frequent Contributor (1K+ posts)
Member # 8165
posted
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
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Lymeorsomething
Frequent Contributor (1K+ posts)
Member # 16359
posted
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
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Marnie
Frequent Contributor (5K+ posts)
Member # 773
posted
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.
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