Tmrwedition.com had an interview with neurologist Andrew Lee. He was asked, what would you do if you had Parkinson’s?
His answer included, drink more coffee and chew nicotine gum a couple times a week. His other advice was “be happy” which is easier said than done and might be indicative of him giving bad advice in general.
Does anyone here chew nicotine gum for PD?
I thought that increased nicotine was protective against developing PD but that once you have it, it’s too late. Anyone know?
It's all a mystery to me, but I think it's reasonable to think things which prevent PD may also slow progression, but nobody really knows. For that matter, I'm not at all sure that nicotine prevents PD -- except that those who die prematurely from lung cancer are less apt to get PD...ugh.
"Our data support the notion that patients with PD are able to quit
smoking more easily than controls. These findings are compatible with a
decreased responsiveness to nicotine during the prodromal phase of PD.
We propose that ease of smoking cessation is an aspect of premanifest PD
similar to olfactory dysfunction, REM sleep disorders, or constipation
and suggests that the apparent “neuroprotective” effect of smoking
observed in epidemiologic studies is due to reverse causation.
...
Twin studies reporting that the twin with PD smoked less than the twin without PD also discredited a simple genetic trait hypothesis.20,21 Furthermore, among twin pairs, the one who developed PD stopped smoking on average 3.7 years earlier than the twin without PD; when both developed PD, the one affected first stopped smoking on average 1.3 years earlier.20 These observations fit the “loss of nicotine reward” hypothesis because one would expect the cotwin who develops PD first to quit smoking earlier. Notably, a similar sequence was observed for loss of smell in these twins: at baseline, the olfactory function of the twin who developed PD was impaired while the cotwin without PD had normal function, and cotwins who developed PD had a greater decline in smell than cotwins who did not develop PD.22 While these twin studies suggest that the smoking–PD associations are not easily attributable to a genetic trait shared by twins, they do not contradict, and even corroborate, the hypothesis that loss of nicotine reward may indicate insidious PD onset similar to loss of smell.
The simplest explanation for the smoking–PD association relates to the sensitivity of the brain reward system in response to nicotine; specifically, it has been suggested that loss or downregulation of nicotinic receptors may precede neurodegeneration.23,24 Postmortem studies of patients with PD have demonstrated a substantial loss of nicotinic receptors in the parietal cortex,25 frontal and temporal cortices, hippocampus, thalamus, striatum,26,–28 substantia nigra pars compacta, and laterodorsal tegmental nucleus,24 leading to speculations that receptor loss might be responsible for cognitive, motoric, and behavioral deficits in PD."
I read the blog post. Clearly she researched a lot but I wonder what her sources are. Have you asked her? Have the lozenges you use been addictive? A neurologist saying he would personally use nicotine makes it very compelling.
It was written by me. If you search pubmed you will find many papers. I no longer have a list of the sources. They are addictive but less than smoking.
Supposedly nicotine ties up nerve endings that are active in PD. Those 'Stop Smoking' skin patches work as well as tobacco. I didn't try them because I don't know whether they're addicting as nicotine is.
Do you have any research or articles on it? The patches are quite a commitment and I’m concerned about addiction too. That is likely why the neuro recommended gum and I think he said a couple times a week
It is not clear if it's effect of nicotine's or some other chemical in tobacco but smokers are definitely have lower risk of getting PD than non-smokers.
My father was a smoker. He smoked since he was 16. When he was in his late 60s although being healthy he was pressured by public opinion and my mother and he quit smoking. In less than 2 years he developed PD, very aggressive form, and he passed away at 76. I believe if he kept on smoking he would not get PD.
Thank you for pointing out that it might not be the nicotine but the tobacco. That would make this doctors advice awful. Coincidentally, my father smoked a pipe up until his 60’s and shortly after quitting he was diagnosed with PD. The correlation had not struck me until just now.
Me again, I am unable to access the link bc it is blocked by adds for a neurology magazine that refuses to close. Please tell me, does the article state that it’s unknown if it’s the nicotine or tobacco?
You cant compare, they are not the same. Nicotine is a drug that stimulates nicotinic acetylcholine receptorsTobacco is a general term for any product prepared from the cured leaves of the tobacco plant.
Yes but what is neuro protective, the nicotine from the tobacco or something else within the tobacco? My intention is to determine if nicotine products would help with PD or if it is something in the tobacco other than or in addition to the nicotine that is protective.
After entering whatever you're searching for, click the "Filter Results" button, then click the dot next to "My Communities." Assuming this is your only community, your search will be limited to posts within the Parkinson’s/Movement Disorders community. Good luck!
The authors state other constituents besides nicotine could be responsible and mention anatabine. Anatabine is an alkaloid derived from ornithine; it sounds like another chemical, agmatine, but agmatine is a biogenic amine. However agmatine is derived from arginine, and ornithine is made from arginine so they are sort of like cousins. The structures look very different, but I noticed both have a double bonded N and a single bonded N on one side. I only had one semester of biochemistry, so I don't know if that means much - but they both share an activity (which I guess is what is important) - they both decrease iNOS activity. Agmatine is an iNOS inhibitor and anatabine downregulates iNOS expression.
It is interesting that agamtine is found in abundance in Japanese sake and rates of PD in Japan are relatively low among industrialized nations, and even more interesting - the sex ratio is flipped (more women than men are affected). I don't know how sake consumption compares between sexes, but women in Japan are more likely to be never drinkers than men.
Thank you. I am awakening to the realization that not only must we advocate for ourselves we must deep dive researchers. This is not a role I’m well suited for but I will do my best. Agmatine is on my homework list now. Thank you for your help.
Some of this might come from a guy who I used to converse with via email. An American. He found his symptoms massively declined when he chewed this gum and researched it. He found that aubergines/egg plant held the same substance and then juiced about 10 of them daily. I tried it but as usual it ‘didn’t work for me’. 😂. I’ll see if I can dig out this guys book for you. He went from 1000 mg of Sinemet to 100/200 a day.
Eggplants? That’s a surprise. Eggplants are high in lectins which are inflammatory and contribute to small intestine bacterial overgrowth. Steer clear of eggplants for a healthy gut biome.
parkinson's ohiohealth There are a lot of videos from neurologists and others working on Parkinson's. This is where I found the video extoling nicotine patches for PD symptom relief but can't find in now.
A few abstracts, all of whom require money to view the full study. There may or may not be much more that is current, at least from organized researchers. No, I can't devote the bucks on these articles, but if someone has active institutional registration they might be allowed to look them over and summarize or paraphrase. Or those of you with a bit more money for this kind of look can take a look and maybe distill something that might make sense for people looking at patches and pills and tobacco (for those who don't want to smoke and risk the cancers, there is always chewing tobacco, that route may be slower for cancer).
Hi, I‘m chewing nicotine chewing gums since I was diagnosed in 2013 - without having smoked ever before.I‘m feeling pretty well, still working (as a TV-Journalist, also filming and editing), playing the piano, doing a lot of exercises and hiking mostly every day....(the only sport I don’t dare to practice anymore is skiing, missing it a lot!!)
I think nicotine chewing gums help me, especially after 3 1/2 hours having had my last Madopar, getting kind of mild dyskinesia. I‘m moving around less...and feel good....
But: If I chew them too much I have to vomit. Never use more than 2 mg, several times a day....
Thank you Davor! Awesome info. I’d really like to hear what else you do or use and how did you arrive at the decision to incorporate the nicotine? It is unknown by most PWP which makes me really curious what else you know!
Dear Cclemonade, I read from studies about nicotine preventing PD, so I started with chewing gums. No idea whether it helps, but especially when my Madopars efficiency comes to an end and I get some kind of Dyskinesia, it helps. Or at least I believe it helps. And believing itself is helping, as we all know, don‘t we? 😀
My father had tobacco sensitivity with his multiple system atrophy - that is, he would get precipitously worse after smoking a cigarette. I have always wondered about the mechanism and whether it was the nicotine or some other substance. Tobacco sensitivity in MSA has been reported in the literature but it is considered rare. I have had periods in my life when I would get sudden onset of lower urinary tract symptoms when exposed to second hand smoke - but other times I did not have that issue. Same thing for coffee (regular or decaf) - which also gives me a noticeable cognitive boost (not worth peeing my pants, though).
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