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.
MAST CELLS
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.
ABOUT MINOCYCLINE
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.
