CLARITIN FOR LYME
You cannot take Claritin to kill Lyme. It has been shown that desloradine, a metabolite of Claritin inhibits the absorption of manganese through the cell membrane of the spirochete. Manganese is used by Lyme bacteria to generate energy in lieu of the iron used by most organisms. In a test tube it works! We have what is called “proof of concept.” Unfortunately the minimum dose of Claritin needed to accomplish this goal is 40 tablets which no one is recommending. Still, it provides a direction for further work.
Why do I recommend Claritin? Although Claritin is a weak antihistamine, it helps inhibit mast cell activation. Whereas Dr. Afrin recommends a slow process of therapy to treat MCAD, mast cell activation disorder, I favor more of a shotgun approach, beginning with numerous agents. My patients are too sick to wait for the slow approach. My patients seem to have something different: a hybrid of chronic infection and excessive mast cell activation These drugs are nontoxic and can always be reduced one at a time when patients improve. The more I have used the therapy the more I have been impressed by its efficacy. (Lists of agents are available elsewhere: also consider doxepin for sleep in lieu of trazodone; very potent antihistaminic effects and possible mast cell effects as well). I do prescribe a lot of Claritin but not to kill Lyme per se.
Mast cells may be the overlooked step child of the immune system. They are everywhere and in close proximity to blood vessels. There are omnipresent and heterogeneous. They serve many functions. For example, the glial-mast cell connection or dialogue. The naturally occurring agent palmitoethylanolamide may be helpful based on recent studies.
More about neuroinflammation. Inflammation is a catch all term. Lyme is a disease of inflammation which translates into some sort of activity of the immune system. Inflammation is not a bad thing in and of itself. Inflammation is needed to fight off infection and for normal “housekeeping” functions of the immune system. It is when inflammation is out of control, like a runaway train that we get into trouble. As a general rule, inflammation can be chronic or acute. Chronic is never good.
The brain is not quite the immune privileged area I have referenced in the past. Glial cells in the brain comprise the resident immune system and they are quite active. Drugs that reduce neuroinflammation and suppress glial cells should be good, right. Not necessarily. Minocycline is touted as having anti-inflammatory effects in the brain. It is an active glial cell inhibitor. Minocycline was studied in patients with ALS. Surprise: patients got worse, significantly so. Glial cell activation is a normal, necessary function. In this case, perhaps changing only one side of the equation caused harm, not good. Care should likely be taken when minocycline is prescribed for long periods of time.
Doxycycline may be different. It may reduce brain inflammation also by a reduction of MMP-3 reducing apoptotic effects. (Cell death) and also have an effect on glial cell activation. As with my experience, the effects of two drugs can be quite different. Although minocycline crosses the BBB better than doxycycycline, I have always found that doxy is the more effective drug. Molecular mechanisms are being worked at by scientist as we speak (and also over my head). As clinicians we need to be mindful or potential distinctions amongst drugs of the same class.
Treatment of excitotoxicity on the other hand appears to always be a good thing, with drugs such as Lamactal and Namenda. Rocephin treats excitotocity so it should not make neuroinflammatory disease worse.
Is it possible that the minocycline is killing bacteria in the ALS patients, which is causing Herx reactions and this, rather than glial cell suppression, could explain the worsening symptoms. In his initial clinical studies, Dr. David Martz has found that patients in early stage ALS can benefit from antibiotics, but in later stages antibiotics (and I don't believe that this was restricted to minocycline), exacerbate their symptoms. Could this be because late stage ALS patients are so compromised that they are unable to detoxify effectively?
Hi there, I'm Lindsey! I have a question and would love to speak with you. Could you please email me when you have a chance? Thanks so much, looking forward to hearing from you :) lindseyDOTcaldwellATrecallcenterDOTcom
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Dr. Jaller, this is Mr. Sindoni, a current patient of yours. After being prescribed mast cell and H1/H2 antagonists, I quickly felt better. I further analyzed my regiment to determine which substances were responsible for this radical change. All of the antihistamines made me feel drowsy and cognitively impaired. Claritin, however, induced a herxheimer reaction (painful arthritis) but alleviated my neurological symptoms temporarily. I found Clairitin alone was responsibile for this feeling. This led me to draw one of three possible conclusions: 1. H1 antagonism was responsible, 2. Borreliacidal action was responsible, 3. Loratadine is structurally related to quetiapine (an anti-psychotic). The effects of multiple other H1/H2 antagonists, and even leukotriene antagonists did not coincide with that of Claritin's; there was no comparison. Additionally, why would an antihistamine simultaneously induce a painful herx yet alleviate my neurological symptoms? No other antihistamine, or antibiotic, has been able to exacerbate my skin rashes, and then have them diminish after 3 days of administration. Finally, the structural relation to quetiapine is so remote that one could assume Loratadine is not efficacious in the treatment of psychotic ailments. After reading the PubMed publication regarding Borreliacidal action of Loratadine, I realized the amounts were far too high for ingestion. Further research revealed at a calculated 100mg bid, Borreliacidal action was observed. Seeing as though 5mg bid had a profound effect, I decided to increase the dosage. After all, we’re discussing a FDA approved OTC medication which has been through clinical trials. Hepatoxcicity seems relatively low, side effects seem controllable, and the ends justify the means. This is a matter of life or death to me. Seeing as I am not a doctor, I do not recommend what I have performed on myself. According to the PubMed findings, 100mg-400mg bid should be effective in treating Borrelia. I saw a glimpse of hope with this medication, and although most of you are thinking my methods/findings are ludicrous, the results do not lie. When you consider suicide because your life has been ruined, this alternative seems like a viable alternative. To mediate possible anti-muscarinic and anti-cholinergic effects, I added Coluracetam (a high-affinity choline reuptake inhibitor) to my regiment. On the second day, I took 50mg bid. After 3 days of treatment, I felt brand new. No neurological symptoms. No pain. Nothing. After ceasing administration of Loratadine, my symptoms do not return, further reinforcing Borreliacidal action to be responsible for my quick change in health. Residual symptoms do exist, but I do not feel strongly enough about them to say I’m still suffering. I am now taking 100mg bid. My body tolerates it well, and for once I do not have a stiff neck, my skin rashes are nearly gone, and I can think clearly! Since the PubMed article does state round bodies were found following administration of Loratadine, I added Flagyl (from an old prescription) to my regiment. I will explain what I’m taking and why: Flagyl kills cystic forms and penetrates the BBB, Quinine eliminates persister cells (according to John’s Hopkins), Loratadine (by far the most effective Borreliacide in my experience), and Minocycline (penetrates the BBB). This combination has rejuvenated me in a matter of 3 days time. I think you should reconsider your ideology behind Loratadine. I know you won’t agree with me, but there is no arguing with the results. The only antibiotic which gave me these same feelings was IV Rocephin, but it ceased to kill Lyme after the first week. You have stumbled upon Lyme’s crutch: Loratadine. Furthermore, PubMed states that other chemicals, such as Yohimbine, which also have affinity for the BmtA transporter were not conclusively effective Borelliacides. Although this could be a direct effect of bioavailability, the study suggest Loratadine may be a Borreliacidal effect for reasons apart from BmtA binding.
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how things are going doc? waiting for a new post. keep up with the good work!
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