Posted 8/3/2011 8:06 PM (GMT -5)
Unfortunately most of the studies are on tobacco which has a boat load of problems within itself:
I Realize that all the information is college level and hard to understand. All neurotoxins such as VX which is a deadly chemical weapon
http://en.wikipedia.org/wiki/VX_%28nerve_agent%29
Chemical characteristics
With its high viscosity and low volatility, VX has the texture and feel of motor oil. This makes it especially dangerous, as it has a high persistence in the environment. It is odorless and tasteless, and can be distributed as a liquid, both pure and as a mixture with a polymer in the form of thickened agent, or as an aerosol. It works as a nerve agent by blocking the function of the enzyme acetylcholinesterase. Normally, an electric nerve pulse would cause the release of acetylcholine over a synapse that would stimulate muscle contraction.
LYME INACTIVATES ACETYLCHOLINE
http://www.lyme-symptoms.com/LymeNeurotoxins.html LINK
The Bb neurotoxin can affect any and all body systems through the inactivation of acetylcholine. When the neurotransmitters, acetylcholine,is diminished and inhibited by the Bb toxin the action of the nerves is sabotaged/interupted such as for the calming of smooth muscle found in the heart,for muscle contraction in skeletal muscles,intestines,and many other parts of the body, including the detoxification organs. (This can further impair or block the route for normal excretion, causing an accumulation of toxins within the body.) The Bb neurotoxin can affect any and all body systems through the inactivation of acetylcholine. When the neurotransmitters, acetylcholine,is diminished and inhibited by the Bb toxin the action of the nerves is sabotaged/interupted such as for the calming of smooth muscle found in the heart,for muscle contraction in skeletal muscles,intestines,and many other parts of the body, including the detoxification organs. (This can further impair or block the route for normal excretion, causing an accumulation of toxins within the body.)
Tobacco smoking may predispose humans to respiratory disease, and may be a compounding risk factor in HIV infection and progression to AIDS. We have demonstrated that chronic exposure of mice and rats to cigarette smoke or nicotine inhibits T cell responsiveness, which may account for the decreased antibody response to T-dependent antigens seen in these animals. This inhibition may result from aberrant antigen-mediated signaling and depletion of IP3-sensitive Ca2+ stores in nicotine-treated animals. Moreover, nicotine appears to moderate the inflammation associated with turpentine-induced sterile abscess and influenza infection. These anti-inflammatory properties of nicotine may account for longer survival of nicotine-treated than control mice lethally infected with influenza virus. However, because inflammation is required for clearance of many pathogens, nicotine-treated mice exhibit significantly higher titers of influenza virus following infection. These results offer an explanation for the higher susceptibility to some infectious diseases, but greater resistance to some inflammatory diseases among human smokers.
The Borrelia burgdorferi bacteria, in their life process (living and dying) release nerve poisons/toxins/biotoxins (similar to Clostridium botulinum) and are believed to be the cause of most, if not all, the symptoms of Lyme disease.
These toxins are dumped into the bloodstream and circulated throughout the body, until they can either be eliminated by the body or get lodged in areas of weakened tissues
http://www.lyme-symptoms.com/LymeNeurotoxins.html LINK
Neurotoxins are attracted to the nervous system, absorbed by nerve endings and travel inside the neuron to the cell body disrupting vital functions of the nerve cell and may lodge there long after the Bb infection is gone.
Neurotoxins are attracted to the nervous system, absorbed by nerve endings and travel inside the neuron to the cell body disrupting vital functions of the nerve cell and may lodge there long after the Bb infection is gone.
http://www.aapsj.org/articles/aapsj0704/aapsj070486/aapsj070486.pdf
The importance of discriminating between the effects of
nicotine versus the effects of tobacco becomes apparent
when examining the literature contributing to the developing
concept of the “ cholinergic anti-infl ammatory pathway, ”
where nAChRs could prove to be valuable targets of therapeutic
agents directed toward mediators of inflammation.
Pavlov and colleagues 42 and Wang et al 43 fi rst reported that
acetylcholine or nicotine pretreatment of human peripheral
blood mononuclear cells acted through a posttranscriptional
mechanism to reduce the amount of tumor necrosis factor
alpha (TNF a ) present in the media 2 hours following stimulation
with the bacterial component lipopolysaccharide
(LPS). The anti-infl ammatory properties of nicotine were
specifi c in that other infl ammatory cytokine production such
as IL-1 b , IL-18, and IL-6 were inhibited but not the antiinfl
ammatory cytokine IL-10. Under normal conditions (ie,
in the absence of nicotine), it would appear that the vagus
nerve release of acetylcholine at sites of peripheral tissue