I cut out a section on Benicar below and wondered if anyone has tried this protocol. According to this doc who also had lyme..
"Benicar is a medical miracle for those suffering with lyme" (see last pp)
A Major Medical Breakthrough; Dr. Trevor Marshall's Angiotensin Discovery
The following discovery by Dr. Marshall shows how a Th1 inflammatory response can become self-perpetuating via the following biochemical pathway.
Please note that sarcoidosis has a very similar pathogenesis to borreliosis. Borreliosis may actually cause many cases of sarcoidosis.
The Angiotensin Hypothesis
New Treatments Emerge as Sarcoidosis Yields Up its Secrets
Trevor G. Marshall, Ph.D.,
We have concluded that sunlight fuels the inflammation of sarcoidosis, via 1,25-D and Angiotensin II, in the following manner:
As the circulating concentration of 1,25-D increases within the inflamed tissue, a much larger quantity of hematopoetic stem cells differentiate to produce monocytes .
Monocyte differentiation into macrophages and epithelioid giant cells is enhanced. The differentiating macrophages and giant cells release Angiotensin Converting Enzyme. This ACE catalyzes Angiotensin I to form Angiotensin II (A-II).
The A-II then binds at A-II Type 1 receptors on the macrophages and activated T-lymphocytes , stimulating Nuclear Factor-kappaB (NF-κB) to signal the release for a cascade of Th1 cytokines .
At least one of these cytokines, Gamma Interferon, increases the amount of 25-D being converted to 1,25-D in the macrophages, which in turn catalyses the differentiation of monocytes into even more macrophages and giant cells.
Normally this inflammatory cycle is self-limiting, but, in the case of sarcoid patients, 1,25-D levels are poorly controlled, leading to upregulated production of monocytes, and their upregulated differentiation into the macrophages and epithelioid giant cells characteristic of sarcoid granuloma.
Reichel, et al, demonstrated that lipopolysaccharide from gram-negative bacteria stimulated the generation of 1,25-D within pulmonary alveolar macrophages from sarcoid patients.
A bacterial pathogenesis is therefore consistent with the initial increase in paracrine 1,25-D concentrations needed to trigger the run-away inflammatory biochemistry described above.
The blockade of A-II Type 1 receptors has been shown (in-vitro) to reduce production of the Th1 cytokines, including TNF-α, an action which would interdict this inflammatory process.
Angiotensin Receptor Blockers are currently indicated for hypertension. There is thus a simple clinical test of this hypothesis available for patients who are suffering both from Sarcoidosis and mild hypertension.
We have found that Benicar (Olmesartan Medoxomil), administered as 40mg every 6 to 8 hours, provides a very effective angiotensin blockade.
There are two issues in the selection and dosage of the ARB. As you can see from the pressor effect vs. dosage for Benicar (Figure 1), about 90% of the ultimate pressor effect can be achieved with only 40mg, once per day. But this dose is not well tolerated by sarcoid patients.
Partly this may be the result of the additional Angiotensin receptors in the inflamed tissues, all of which have to be blocked, and partly it may be due to an increased production of serum ACE by macrophages in response to the partial blockade.
Sarcoid patients experience symptoms ranging from increased fatigue to psychedelic dreams when prescribed ARBs just once daily, the customary prescription for hypertension
To be fully effective, we found that Benicar must be prescribed to sarcoidosis patients as 40mg every 6 to 8 hours. We found the ARB Diovan (Valsartan) to be less effective than Benicar, but it may be used at the 80mg q8h described in our earlier paper.
Two patients reported sinus congestion with the Diovan blockade, which was not present after changing to Benicar. Controlled studies are needed to accurately define the blockade capability of each ARB, individually and in combination.
In summary, Dr. Marshall's discovery reveals that during the pathogenesis of borreliosis the BLPs of borrelia trigger inflammation via TLR signaling pathways or by other intracellular activation of NF-kappa B, which stimulates the gene expression for inflammatory cytokines. When the inflammatory cascade goes chronic, it eventually goes into the self-perpetuating cycle described by Marshall. This cycle will continue to produce disease until it is stopped by intervention.
In my opinion, Dr Marshall's discovery that A-II perpetuates a TH1 inflammatory cascade is nothing short of major medical breakthrough.
Dr. Marshall's work has not only given us the model for the pathogenesis, he has also given us the therapeutic approach that breaks the perpetual cycle that maintains the inflammatory cascade.
Angiotensin II type 1 receptor blockade. The angiotensin receptor blocker (ARB) called Benicar (olmesartan medoxomil) has specific ARB properties that block this self-perpetuating inflammatory cascade.
Benicar therapy is a medical miracle for those suffering with chronic borreliosis.
-------------------- We are spiritual beings on a human journey...
-------------------- Suzanne Shaps STAND UP FOR LYME Texas (www.standupforlyme.org) (Please email all correspondence related to protecting Texas LLMDs to [email protected] with copy to [email protected]) Posts: 977 | From Austin, TX, USA | Registered: May 2004
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