This one is a bit technical. You can skip to the bottom.
Neuroborreliosis the most common and dreaded syndrome I see in patients with disseminated Lyme disease is amongst the most challenging clinical problems seen.
Some mechanisms of CNS dysfunction have been fairly well demonstrated. Bb can cross the blood brain barrier. The pathogens are greeted by local immune cells including: monocytes, macrophages and dendritic cells. An inflammatory reaction medicated by cytokines and chemokines is initiated. Antibody producing B cells appear in the CSF(spinal fluid) in unexpectedly high numbers. The Bb bacteria seem to enter glial cells(supporting cells) rather than brain neurons. A proliferation of killer T cell(clones) has been shown. The damage to nerve cells seems to be due to cytotoxic(cell killing)side effects of this process. Autoimmune processes via the production of autoantibodies and molecular mimicry have been established in animal models. The third purported cause of Lyme/brain disease involves "neurotoxins." From what I can gather, this seems to be a theoretical idea; there is not much science to support it.
The most frequently mentioned neurotoxin is quinolinic acid. High levels of this toxin have been measured in the spinal fluid of patients with various chronic neurological diseases. There is experimental evidence that macrophages incubated with Bb produce quinolinic acid. Scientific evidence, from my review of the literature, does not support the accumulation of quinolinic acid in the brains, spinal fluid or bile of Lyme patients. If such evidence exists please post it here.
The neurotoxin theory, as it relates to bile acid sequestrants is:
Lipid soluble toxins are postulated to be processed through the liver, then end up in bile, which is recirculated. These toxins are then able to egress back into the blood stream, find their way past the blood brain barrier and cause neurological dysfunction. These toxins have not been identified. Bile binding resins remove these toxins causing an improvement in neurolgical dysfunction.
These ideas stem from theories described by Dr. Shoemaker in Maryland. And have been repeated by Dr. Burrascano in his guidelines.
Standing back, the theory seems dubious at the very least.
In my clinical practice I have tried these drugs: they work! How?
It turns out that Welchol lowers CRP- C-reactive protein, a primary marker for inflammation or immune activation. CRP is a circulating protein which initiates the complement cascade. This a major "effector" mechanism of the immune system.
Rather than removing neurotoxins, Welchol may be removing inflammatory byproducts of the immune response to Lyme infection. This dovetails with my observation that this drug frequently reduces not only brain inflammation, but can frequently improve other immune mediated symptoms like joint pain.
Bottom line: Welchol and Questran help. They remove "something" that is bound to bile, or by some other mechanism. They lower inflammation based on studies which show a reduction in CRP.
Food for thought: Statin drugs like Lipitor also lower CRP. This mechanism in the prevention of heart disease may be more important than the cholesterol lowering effect. Some studies have shown that patients on statins have a lower rate of Alzheimer's disease. Anti-inflammatory effect? "Neuroprotective" effect?
Better news. Coffee is the new wonder drug. It lowers the risk of Parkinson's, Alzheimer's, liver disease and more. It apparently reduces brain inflammation.