Sometimes you do a better job when you don't know what you are doing. As I started treating Lyme disease my mentor told me that vitamin D was low. It should be checked and replaced. I dutifully checked vitamin D OH 25 and found it to be uniformly low. I immediately started new Lyme patients on high dose pulses of vitamin D. In retrospect they all did well with this approach. Then I learned I wasn't supposed to do this. The patients were vitamin D toxic. When I checked vitamin D dihydroxy 1,25- the active form,I found that sure enough, the patients were really vitamin D toxic! Now I told my patients to withhold D and even consider Benicar. This was based on theory- not practice.
What if I was right the first time?
One huge problem with Lyme patients is that they don't make antibodies against the germ. In technical terms there is a poor humoral response.
What have we (I) learned? Lyme is a Th1 disease associated with a shift away from Th2. This describes a helper T lymphocyte response. (If you don't know what that means you can still follow the gist of this blog). The Th2 response is needed to promote antibody production. These Th1 weighted patients need a push in the Th2 direction to gear up the antibody making machinery. Vitamin D helps with this according to my immunology text.
Maybe high/toxic vitamin D levels are a good thing. Maybe they help (in lingo) up- regulate immunological receptors which would increase antibody production, a major thing that is missing in Lyme patients!
Maybe it is particularly useful to give extra D when antibiotics are first prescribed and a Herx occurs. This might be a critical chance to influence ongoing and future production of antibodies directed against Lyme.
All of the above is wild speculation and based on a logical argument which may be filled with flaws. Really the point is we don't know what we are doing with vitamin D; and, how did a theory from a non physician, about a disease other than Lyme disease, become so influential amongst LLMDS and the Lyme community at large?