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Nicotine and choline supplementation for focus/concentration?


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#1 freizeit

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Posted 15 March 2010 - 10:32 AM


I'm an ex-smoker who has recently started to use nicotine again (in the form of a 7mg patch, possibly moving up to 14mg) to help with focus and concentration as I write my dissertation. My specific question is this: can nicotine be taken in combination with a choline source (e.g., high choline lecithin) without problems? Or should smokers or other nicotine users avoid choline supplementation? I'm very curious to hear from those who have taken choline supplements either while on the patch (for prolonged periods of time) or while smoking.

Here's some background to my question. Prior to starting the patch, I went to my doctor to see what she recommended for focus and concentration. I didn't officially qualify for a diagnosis of ADHD, but I was told that I had "symptoms of ADHD", and I then began a three month period in which I tried Concerta, Adderall, Vyvance, and finally Provigil. The amphetamine-based stimulants worked really well for 4-5 days and then gave me an unbearable spacey/brain-foggy feeling I've never experienced before in my life. If I persist in taking the stimulants through the spacey brain fog, they end up making me feel sick. At one point I was sick for a whole day after taking only 2.5mg of Adderall IR. I've come to suspect that I'm one of the 6-10% of Caucasians who are so-called 'poor metabolizes' of 2D6 substrates, of which amphetamine-based stimulants are one. (If anyone else has had a similar experience with the stimulants, I'd also be interested in hearing about that.) My doctor then gave me Provigil, which at first didn't seem to have an effect at all, and then, at a higher dose (300mg/day), caused some serious anxiety. It's possible that I increased the dose too quickly or didn't give it enough time to work; nonetheless, it wasn't a good experience. So, after my experiments with these medicines, I decided to go back to what had worked for me in the past: nicotine.

But in the process of learning about the substances that I was taking, I also learned about the wide array of nutrients and supplements that can help with focus and concentration. For the past two months, I've been taking a standard multivitamin, a low-dose multi-mineral, and fish oil (1200mg EPA, 600mg DHA) everyday. On top of that, I've recently started to take high choline lecithin (840mg phosphatidylcholine/day) because, according to what I've read, lecithin has a number of health benefits and can help with focus and concentration. For this same reason I'm also interested in other choline sources (e.g., Alpha GPC) but don't know if these can be taken with nicotine or not. I should add that I'm a 30-year-old male in generally good health.

I've tried to do my homework by searching through the forums, but the topic of nicotine and choline rarely comes up. Any experiences or advice would be appreciated.

#2 Imagination

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Posted 15 March 2010 - 07:33 PM

I smoke, well used too, but still on the NRT. I don't tend to react well to choline supplementation well at all. Get depressed/pissed off usually. I keep trying on many occasions but with the same results, i've never really equated the two though, also tried choline when i've been off the nicotine for months with the same results.

I find tyrosine the best for focus and concetration. My memory is usually pretty good.

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#3 hamishm00

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Posted 15 March 2010 - 09:30 PM

I've taken choline (CDP) in large doses with nicotine as well.

I've decided after a 4 week run on Nicotine, although a nootropic, nicotine is evil. The vasoconstrictive effect can't be good, for kidneys, arteries, blood pressure, heart beat. I find it also amplifies anxiety and stress.

Switched to LEF cognitex for my nootropic boost + ALCAR arginate, bacopa and rhodiola.

#4 freizeit

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Posted 16 March 2010 - 03:27 AM

hamishm00, did you always take nicotine and CDP-choline together or did you try them separately as well? In your experience how do the two interact?

I agree that nicotine isn't a great long-term nootropic, but in my case, having smoked regularly for about 8 years, it's highly effective and helps with anxiety, mood, focus, etc. Eventually I'll stop the patches (again), but in the meantime I'm interested to learn more about the interaction of nicotine with other nootropics.

#5 hamishm00

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Posted 16 March 2010 - 09:47 AM

I have of course taken them separately in varying doses - CDP Choline 750mg separately and also 2 x 4mg nicotine gum separately. I've also combined this stack. The results? I find its difficult to notice the nootropic effect of CDP Choline when combined with nicotine. I think it has a lot to do with the CNS stimulation of nicotine, makes it hard to notice anything but that. Its very difficult to say whether or not the CDP actually adds any nootropic benefit over and above the nicotine.

Without nicotine, the CDP effect is noticeable. Especially with clarity of thought, vision and colour perception. As well as keyboard typing accuracy.

I have been nicotine free for two days now, and let me tell you this is a much better world to be in.

My 'brain' supps current stand at:

LEF Cognitex - 3 caps in the morning on empty stomach, maybe 3 in the afternoon (no need to take CDP Choline, this badboy has Alpha GPC which I will rely on for now)
450mg Bacopa - morning, empty stomach
625mg Rhodiola - morning, empty stomach
3 grams LEF Super Omega 3 with Olive extract and Sesame - at night
Perika (Hyperforin + Hypericum) - 1 tab twice daily morning and afternoon
Sam-E 600mg per day (morning, empty stomach)
Phosphatidylserine 100mg, over and above the 200mg in the Cognitex
Acetyl-L-Carnitine Arginate 2.5 grams (morning, empty stomach)
Melatonin - 2mg (at night)

This is a powerful brain focussed regimen IMO. Key markers of nootropic activity I can confirm anecdotally: sharper and quicker access of short term memory, reaction time, peripheral perception, colour perception, sharpness of vision, lucid speech and reduced anxiety.

I have absolutely no need for piracetam, oxiracetam or aniracetam which after many years of use I have found to be not worthwhile as a nootropic. I'm not saying it doesn't have some benefit, but it's hardly what it's hyped to be.

#6 nito

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Posted 17 March 2010 - 03:54 AM

damn gotu kola on an empty stomach hurts.

#7 Imagination

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Posted 17 March 2010 - 08:03 PM

This explains why i don't really react well to choline, if the nicotine plus the choline is too much. Would choline be a good supplement to take for nicotine withdrawal do you think?

#8 Climactic

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Posted 21 August 2012 - 06:55 AM

Would choline be a good supplement to take for nicotine withdrawal do you think?

I naively believe so, because nicotine binds to some of the same receptors (nAChRs) as acetylcholine. However, this assumes that nicotine withdrawal (not to be confused with smoking withdrawal) exists at all. In any event, it may not be a sufficient solution.

Edited by Climactic, 21 August 2012 - 06:58 AM.


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#9 Ruth

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Posted 23 December 2017 - 03:32 PM

https://www.scienced...166432808001186 Living in an enriched environment (EC) during development enhances memory function in adulthood; living in an impoverished environment (IC) impairs memory function. Compounds previously demonstrated to improve memory among IC rats include CDP-choline and uridine monophosphate (UMP). Brain phosphatidylcholine (PC) synthesis utilizes both the uridine formed from the metabolism of exogenous CDP-choline and UMP, and the choline formed from that of CDP-choline. It also uses the polyunsaturated fatty acid (PUFA) DHA, a precursor for the diacylglycerol incorporated into PC. DHA administration also improves cognition in young and aged rodents and humans; its effects on cognitively impaired IC rats have not been characterized. We have thus examined the consequences of administering DHA (300 mg/kg) by gavage, UMP (0.5% in the diet), or both compounds on hippocampal- and striatal-dependent forms of memory among rats exposed to EC or IC conditions for 1 month starting at weaning, and consuming a choline-containing diet. We observe that giving IC rats either dietary UMP or gavaged DHA improves performance on the hidden version of the Morris water maze (all P < 0.05), a hippocampal-dependent task; co-administration of both phosphatide precursors further enhances the IC rats’ performance on this task (P < 0.001). Neither UMP nor DHA, nor giving both compounds, affects the performance of EC rats on the hidden version of the Morris water maze (P > 0.05), nor the performance by IC or EC rats on the visible version of the Morris water maze (all P > 0.05), a striatal-dependent task. We confirm that co-administration of UMP and DHA to rats increases brain levels of the phosphatides PC, PE, SM, PS, PI, and total brain phospholipid levels (all P < 0.05), and show that rearing animals in an enriched environment also elevates brain PC, PS, and PI levels (all P < 0.01) and total brain phospholipids (P < 0.01) compared with their levels in animals reared in an IC environment. These findings suggest that giving DHA plus UMP can ameliorate memory deficits associated with rearing under impoverished conditions, and that this effect may be mediated in part through enhanced synthesis of brain membrane phosphatides.

https://www.jlr.org/...44/8/1545.short Because brain membranes contain large amounts of docosahexaenoic acid (DHA, 22:6n-3), and as (n-3) PUFA dietary deficiency can lead to impaired attention, learning, and memory performance in rodents, we have examined the influence of an (n-3) PUFA-deprived diet on the central cholinergic neurotransmission system. We have focused on several cholinergic neurochemical parameters in the frontal cortex and hippocampus of rats fed an (n-3) PUFA-deficient diet, compared with rats fed a control diet. The (n-3) PUFA deficiency resulted in changes in the membrane phospholipid compositions of both brain regions, with a dramatic loss (62–77%) of DHA. However, the cholinergic pathway was only modified in the hippocampus and not in the frontal cortex. The basal acetylcholine (ACh) release in the hippocampus of deficient rats was significantly (72%) higher than in controls, whereas the KCl-induced release was lower (34%). The (n-3) PUFA deprivation also caused a 10% reduction in muscarinic receptor binding. In contrast, acetylcholinesterase activity and the vesicular ACh transporter in both brain regions were unchanged.

Thus, we evidenced that an (n-3) PUFA-deficient diet can affect cholinergic neurotransmission, probably via changes in the phospholipid PUFA composition.




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