Well, from what I could find on the internet as far, the studies are very sparse and I was yet to find one that had specifically tested nicotine to see if the disease kept advancing or not. The only study I found talked about someone chewing tobacco, and further studies that cited that one made the false distinction of chewable tobacco as only nicotine.
From the studies that I've found, which helped explain in part how the disease works, I took this information and combined it with what i've learned so far from med school and this is a summary of what I think of this problem:
Buergers disease is an immune condition coused specifically by an antigen in the tobacco plant, that if smoked, or chewed enters in the blood. Although it has weak antigenic properties, it stimulated the immune system specifically in the capillary region, where blood circulates more slowly than in the big arteries (like the aorta or the arterioles). This gave me the clue that this substance is relatively large in size as it doesn't cross the vascular wall, because otherwise it would get an immune reaction going in the tissue also, but Buerger's disease is almost exclusivelly a vascular condition at it's roots. This was the first indication that that antigen was almost certainly not nicotine, as nicotine has a very small relative molecular size.
The immune system starts an immune reaction in the capillary region, and then thromocytes start morphing together and creating thrombuses, as well as the couagulation cascade being activated (fibrin is a pillar of the immune system and of inflammation).
Because of nicotine's small molecular size, not only is it capable of traversing the capillary wall very easily compared to most antigens, it is also too small to exert antigenic properties, that is to bind to an antibody and form an immune complex. Even compared to meds, nicotine has a very small size (that is why it can get through the blood brain barrier and cause all the psychologic effects), and molecules of that size are nonimmunogenic.
Some very strange facts, which (because I am a stark person) lead me to believe that nicotine is almost certainly not the underlying cause of this disease is:
1. it was incriminated in a lot of studies, but those cited other studies to support that fact, and that other studies were allways talking about something else (several studies said that nicotine could be the cause, and for that cited other studies that talked in fact about chewable tobacco); futhermore, all studies stated in the end that the antigen was yet to be found (then why incriminate nicotine) - so there was a dissimulation going full on from what I could tell.
2. there wore no studies in which doctors continued to give their patient which had buerger's only nicotine to test the hypothesis. They could have done this safely because after givimg up om tobacco, the body clears capillaries that are not fully thrombosed. So they could let their patients off tobacco for some time, than only introduce nicotine and see if the condition reactivates, and then quickly stop nicotine. There could also be animal model studies, which have also not been done yet, or cell culture studies from patients............. -weren't they supposed to find the culprit already ??
Some people said that nicotine could be the cause because it is a potent vasoconstrictor ( and adding to it that the whole vasodilation/vasoconstricion debucle is also complicated, because never does the body do vasoconstriction in all areas -when muscle arteries vasoconstrict, organ arteries vasodilate, most notably thr brain, and vice versa; the brain's arteries very rarelly vasoconstricts, and only to a minor degree, because it is a critical region).
So while nicotine generally being a vasoconstricting substance, this disease is all about an immune reaction that activates the coagulation cascade , which in turn ends up clogging arteries. Capillaries don't constrict as they don't have muscles, only bigger arteries and arterioles leading to the capillaries. But visually, even if it was the case, after the nicotine's effects dulled down, the arteries would vasodilate and the blood clot would advance it's way further.
The only other possible way for this immune reaction to occur would be if the endothelial cells (cells that line the vascular wall) would get damaged, and fast (lile in a lot of antigen that would bind to the cells and destroy them or a lot of smoking), and the inside contents of that cell would get released outside and start an immune reaction. While this is also an alternate explanation for this disease, still, nicotine also doesn't damage any cell in the organism in any way. The effects it has are because of it binding to different receptors in the organism. It is a pretty "inert substance".
If it were for me, I would start studying the relation between this disease and nicotine asap, as NRTs and particullarly electronic cigarettes are a very good alternative to smoking, are the best "gateway" to stopping tobacco addiction altogether. The e-cig has always intrigued me, because as I once put it, it's a modified asthma inhalator that could save a billion lives.
This is the link to the o only two cases I could find that specifically talk about this subject: in the first case, i thinl the person stopped vaping before he/she could figure out it's profile related to the disease, and in the second case I would like to note that she didn't tell if she was also diagnosed with buerger's, or if she made that assumption. They are both pretty good reads:
1.
Vaping over analogs ..... Something you should know.
2.
Real Stories - Jennifer Berger Coleman - Part 1 | Five Pawns Blog
