- This topic has 24 replies, 7 voices, and was last updated 2 years, 9 months ago by Ferret. This post has been viewed 4133 times
- April 24, 2018 at 9:19 am #5330FerretModerator
There are too many variables to be cherry picking. This=That simply does not apply with ANYONE.
Above all, a healthy lifestyle is the backbone of treatment for PWN. That includes no sugar, no salt, no alcohol, no fast food and fresh (not packaged) wherever possible.
Getting a baseline for body chemistry is important because it will help you to note trends in the bloodwork and BP. At nearly 67, all my bloodwork is just tickectyboo.
I know what controls my cataplexy and I know what controls my EDS. It’s been a long haul and will be different for everyone.
Nicotine has been documented to work. Period. Will there be side effects? Possibly. It’s up to the individual to monitor their own health and reactions.April 24, 2018 at 1:23 pm #5337Pereise1Participant
Well, to add a possible strategy, I was investigating how exactly Nicotine ups Orexin expression and I found this:
The hypothalamus is a prominent central site of action of nicotine but the phenotype of nicotine-sensitive neurons in this region has not been fully described. Hypothalamic orexin neurons are important regulators of state-dependent behavior, arousal and feeding. Here, we treated rats with acute nicotine and quantitated Fos expression as a marker of neuronal activation. Nicotine increased the percentage of orexin neurons expressing Fos without a significant effect on non-orexin neurons. This effect was attenuated by the nicotinic antagonists mecamylamine and dihydro-beta-erythroidine, implicating α4β2-containing nicotinic receptors. The orexin system is likely to play an important role in the coordination of physiological and behavioral responses to acute nicotine treatment.
So the effects seem to be mediated by the α4β2 nicotinic acetylcholine receptors. So theoretically, things that increase those receptors should be good for us overall. I haven’t been able to use my nicotine patches for more than an hour lately, as I’ve been getting massive amounts of side effects for some reason. Well, after some light investigation, it seems that the common Alzheimer’s drug and natural phytochemical Galantamine potentiates the positive effects of Nicotine by being a positive allosteric modulator on the α4β2 nachr:
Galantamine (Reminyl), an approved treatment for Alzheimer’s disease (AD), is a potent allosteric potentiating ligand (APL) of human alpha 3 beta 4, alpha 4 beta 2, and alpha 6 beta 4 nicotinic receptors (nAChRs), and of the chicken/mouse chimeric alpha 7/5-hydroxytryptamine3 receptor, as was shown by whole-cell patch-clamp studies of human embryonic kidney-293 cells stably expressing a single nAChR subtype. Galantamine potentiates agonist responses of the four nAChR subtypes studied in the same window of concentrations (i.e., 0.1-1 microM), which correlates with the cerebrospinal fluid concentration of the drug at the recommended daily dosage of 16 to 24 mg. At concentrations >10 microM, galantamine acts as an nAChR inhibitor. The other presently approved AD drugs, donepezil and rivastigmine, are devoid of the nicotinic APL action; at micromolar concentrations they also block nAChR activity. Using five CHO-SRE-Luci cell lines, each of them expressing a different human muscarinic receptor, and a reporter gene assay, we show that galantamine does not alter the activity of M1-M5 receptors, thereby confirming that galantamine modulates selectively the activity of nAChRs. These studies support our previous proposal that the therapeutic action of galantamine is mainly produced by its sensitizing action on nAChRs rather than by general cholinergic enhancement due to cholinesterase inhibition. Galantamine’s APL action directly addresses the nicotinic deficit in AD.
Edit: Here’s another few. I’ve only tried Galantamine which definitely helps with the cognitive dysfunction that N gives:
Nefiracetam has been shown to potentiate ACh currents in the α4β2 receptor of rat cortical neurons with a bell-shaped dose–response relationship and the maximum effect at 1 nM. This effect was exerted via Gs proteins. The α7 receptor was almost unaffected by nefiracetam. Nefiracetam also potentiated NMDA currents with the maximum effect at 10 nM via interaction with the glycine-binding site of the receptor. Galantamine had a moderate potentiating effect on the α4β2 receptor and potentiated NMDA currents with the maximum effect at 1 μM. However, galantamine did not interact with the glycine-binding site. Donepezil, a potent anticholinesterase, also potentiated NMDA currents at 1—10000 nM. In conclusion, these three drugs potentiate the activity not only of the cholinergic system but also of the NMDA system, thereby stimulating the downregulated nACh receptors and NMDA receptors to improve patients’ learning, cognition, and memory.
I’m trying to find a source for Nefiracetam and I’ve ordered Donepezil, which should arrive sometime next week.April 24, 2018 at 1:30 pm #5339JasonKeymaster
When you consider anticholinergic medications increase the risk of dementia, it makes a lot of sense that nicotine or similar substances might be helpful. Smoking, on the other hand is linked to increased risk – probably because it causes vascular damage and other issues. I couldn’t find any studies regarding pure nicotine in dementia prevention but that’s a relatively new thing. Now that vaping is so popular, umm maybe in 50 years, we’ll have some evidence 🙂April 24, 2018 at 2:04 pm #5341FerretModerator
Jumpin’ Jehosaphat Guys! Go back to the very first post in this thread. EVERY link in the second part (except the first and the last) mentions the positive effects of Nicotine on Alzheimer’s.April 24, 2018 at 5:39 pm #5345TheRabbitKingKeymaster
Interesting that you skipped over the elephants in the room (marked increase in simple/refined carbohydrates and overall caloric intake in NA diets) in your attribution to diabetes rates.
I’m sure you can find nicer graphs noting the trend between carbs and obesity/diabetes.
If you want to keep using nicotine as an upper, sure go ahead. Ignore/don’t care to understand what insulin resistance means -meh.
As admin/senior members of this group – keep in mind you may be contributing to future adverse health outcomes, for a group of people already at risk. By virtue of our disease we are already at increased risk of metabolic syndrome and insulin resistance. The unbalanced ‘pro-nicotine’ posts I’ve seen irked me enough to join just to post a counter point.
Sorry drugs are different, and their pros and cons will differ in their magnitude and efficacy. If you don’t understand, then learn. 30 years from now when they find a cohort of pwn with increased rates of diabetes – part of that blood will be on your hands.
Please keep hyperbolic vitriol to a minimum please. This is a support forum. If you believe someone is misrepresenting themselves as a medical professional and handing out bad advice, feel free to report them to me, as that crap will not be tolerated, but otherwise I want people to feel free to share what has helped them without having being excoriated
My current jam: Anathema - SpringfieldApril 24, 2018 at 6:37 pm #5347Pereise1Participant
Jumpin’ Jehosaphat Guys! Go back to the very first post in this thread. EVERY link in the second part (except the first and the last) mentions the positive effects of Nicotine on Alzheimer’s.
No doubt, however, my post was in regards to potentiating the pro-orexin effect with Galantamine. If I’m not mistaken, it’s OTC in Mexico right? It’d be interesting if it potentiates the therapeutic effects of nicotine for you.April 24, 2018 at 6:46 pm #5349FerretModerator
Thanks Pereise 1 but I like my rut exactly as it is. I don’t feel the need to add anything else to my regimen right now. Sorry.April 25, 2018 at 9:36 pm #5385JasonKeymaster
@ferret Haha, pereise and I are willing to try just about anything. On a side note, because of the big debate on nicotine, I figured I’d mention that regardless of anyone’s opinion on nicotine as a treatment, Ferret bringing it up and talking about it on this thread made a new undiagnosed member find us on Google when searching for nicotine and cataplexy and has helped send him on the path to diagnosis, which is pretty awesome. Most clinicians and no one without N/IH is going to have that sort of practical insight. Credit goes 100% to Ferret for changing a life.May 28, 2018 at 7:50 pm #5765mesleepyParticipant
Hello having a tuff time with my narcolepsy
I was diagnosed at 11yrs old an was given Retilin for 4yrs never did like then to cylert (May have that spelt wrong) 2yrs
At 16yrs old become a full time smoker not taking meds regularly
By the time I was 18yrs old no meds going to secondary education sleeping in class an awake for shop 50/50
Up until now held full time job an drivers license
Then all hell I quit smoking
I quit cause of cost $500 a month
Been 6months not working cause dr can’t get me medication to work going through new sleep study no records cause hasn’t been issue till now 20yrs
If I could afford it I’d go back to smoking
Grrr now taking toll on mental healthMay 28, 2018 at 9:21 pm #5769FerretModerator
Then try vaping. I’ve now been vaping since 2013. Used to smoke about two packs a day. I use about 1 ml. of e-liquid per day and it contains 18% nicotine. Same effect as smoking on EDS and cataplexy but CHEAP.
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