nicotine, You could test nicotine patches... - Cure Parkinson's
nicotine, You could test nicotine patches to see if it has a positive effect on Parkinson's. Or?
(Edited) prior to having access to the article in English, I thought niacin might play a role in nicotine’s positive effect. I was wrong. But, nicotine and niacin are analogous and the latter effects the former. Nicotine decreases NAD levels. Something to consider if considering using nicotine for PD.
Original comment: Nicotine and nicotinic acid sound similar for a good reason. Why not increase nicotinic acid intake? The humble and important niacin! 😊Can anyone translate the article? I would like to read it.
Nicotine on prescription?Nicotine is addictive and is partly responsible for the health damage caused by smoking. However, the active ingredient can also increase cognitive performance and is therefore being tested as a therapeutic agent for some neuropsychiatric diseases.
In the summer of 1926 an article appeared in the British Medical Journal by physician Henry Moll of the University of Leeds, in which he described nicotine injections as a treatment approach for post-encephalitic Parkinson's syndrome. After inflammation of the brain tissue, those affected suffer from symptoms that are similar to the restricted mobility in Parkinson's disease. However, this usually only affects one side of the body. Although he could not have cured the patients, according to Moll, his therapeutic approach would at least alleviate their symptoms significantly. He therefore advocated further research into the method.
In the decades that followed, however, little attention was paid to the therapeutic potential of nicotine. Instead, the professional world collected more and more evidence of the massive harmful effects of cigarette smoking and the addictive potential of the alkaloid nicotine (see »The dark side of nicotine«). In 1966, the epidemiologist Harold Kahn from the National Institutes of Health was not surprised when he analyzed the medical data of almost 300,000 war veterans and the already known connection between smoking and various types of cancer as well as a shortened life expectancy was confirmed again and again. Another result of the study, on the other hand, was quite unexpected: Apparently, non-smokers develop Parkinson's three times more often than smokers. Should there be a substance in the tobacco smoke that protects those affected from the progressive degradation of the brain matter?
In fact, this question has not yet been conclusively answered. In the meantime, however, a number of findings indicate that the nicotine contained in smoke has both a protective effect and a therapeutic benefit in the disease. For example, all epidemiological studies that have been carried out on this have shown that tobacco users are less likely to develop Parkinson's disease.
In 2007, Maryka Quik of the Parkinson's Institute in Sunnyvale, California, treated squirrel monkeys with Parkinson's disease with nicotine. After eight weeks, the animals performed only half as many involuntary movements as before the start of treatment. Because of such promising results, the method was tested on individual Parkinson's patients. As a rule, they were given the substance via plasters. In fact, in many cases, the mobility impairments were reduced.
The problem: not everyone responds equally to the material. In addition, the reasons for the therapeutic effect remain unclear, which complicates the development of drugs. Laboratory experiments at least suggest that nicotine protects the brain from neurotoxins. Presumably, to some extent, it can keep certain neurons that make the neurotransmitter dopamine, which play a key role in controlling muscle movement, from dying down. In Parkinson's patients, these "dopaminergic" brain cells die off, leading to the motor deficits typical of the disease. In addition, the nicotine receptors stimulate the release of the neurotransmitter dopamine and could thus counteract the neurotransmitter deficiency caused by the disease.
Improved brain powers
The fact that nicotine can have a positive effect on the brain is now quite well documented. In 2010, a US working group led by Edward Singleton from Stevenson University in Maryland analyzed the results of 41 nicotine studies from 1994 to 2008. The subjects were given the alkaloid mostly in the form of nasal sprays, patches or injections. The evaluation showed that the substance improved fine motor skills, attention, reaction times and short-term and working memory in the short term compared to a placebo in both smokers and non-smokers. Tobacco companies were only involved in the financing of three of the studies evaluated, but this was explicitly denied in 31 studies, which speaks sufficiently for the credibility of the results (see also "Who financed it?").
Try nicotine patches or gum.
I’m concerned about the nicotine’s effect on the oral and gut biome. I linked what I could find on that.
Patch sounds interesting.
Are you interested in it?
CC, as trials indicated not everyone responds favorably to nicotine. Having read the French doctor's success with nicotine patches (if I remember correctly), I discussed it with my husband and asked him if he would be willing to try it (that was 4 years ago). The experiment failed! He experienced heart palpitations and his BP reached very high! We stopped the experiment as you can imagine. About 1-2 years ago, he tried nicotine gum, but he stopped it, too, as he complained that it burned his throat.
I wish there were black and white answers to our questions on what is the most effective treatment for PD. Look at your supplements/vitamins list and try to identify what are the most helpful ones. I personally have added every supplement we have discussed in this forum in hopes that something will click!
Niacin is created from a process involving nicotine.
lifespan.io/news/a-summary-...
ajmc.com/view/daily-niacin-...
Nicotine is shown to decrease NAD. (I posted a about this)
As your article states, NAD is extremely important.
If one was to use nicotine for it’s possible benefits I think supplementing with more niacin or other NAD precursors would maybe be needed.
'Niacin is created from a process involving nicotine.'
Many words seem alike, but are quite different. My understanding is that this is a case of mistaken identity. Nicotinic acid (also called niacin, as well as vitamin B-3) has nothing to do nicotine.
And while I only scanned your reference, I could not find support for your statement.
Having read the article in its entirety I see the mix-up.
In the article -
'Niacin...can be created by the oxidation of nicotine with nitric acid.'
So while 'nicotine and nicotinic acid sound similar for a good reason' because you can derive one from the other they are not the same.
The focus in this thread here is on nicotine found in tobacco. It bears no resemblance to Niacin.
Sorry Casey but I read additional sources and I believe I am correct. Please see my response with a link and a screen shot showing why.
I know you will kindly inform me if I am wrong and I appreciate that! Together we learn and grow and I appreciate learning from you.
Epidemiological studies have shown smokers have a lower risk of PD. These studies search large data bases for a few criteria with disregard to other valuables. Smokers diagnosed with PD vs. Nonsmokers with PD (as an example) with no consideration of their age at death or what they died of. It could also be smokers died of lung cancer before being diagnosed with PD which would lower the risk of the of the results.
I read on a post (Smokers diagnosed with PD vs. Nonsmokers with PD) 3 times less risk. WOW, maybe I should reconsider. added to post 02/27/22
Disclaimer: I have no idea of the valuables/criteria of the computer searches. Just a question you should think about. I also, have no problem with a concluding: Nicotine triggers a release of dopamine, therefore the continual releases of dopamine has fought off the death of dopamine producing cells.
Nicotine promotes neuron survival and partially protects from Parkinson’s disease by suppressing SIRT6 2018 actaneurocomms.biomedcentra...
Additional quote.
..but this is precisely the point.
You do not want an association between nicotine and nicotinic acid - the vitamin. Thus the words NIcotinic ACid vitamIN became Niacin.
When you react two substances, say nicotine and nitric acid, you get an entirely different compound, with properties unrelated to either of the compounds from which you started.
This is elemental chemistry.
Thank you for your patience and info. I’m still not getting it despite it being “elemental chemistry. “ I’m not trying to be stubborn. I just still don’t understand how your point disproves mine when I’m quoting reputable info.
So, I will do my homework and hope to understand.
All you need to know is this:
When you react two substances, say nicotine and nitric acid, you get an entirely different compound, with properties unrelated to either of the compounds from which you started.
There is nothing to understand here. The statement referenced here is a fact.
Nicotine decreases NAD levels. I don’t know how much. 🤓. So, There IS an association, a negative one. That is very relevant.
Screen shot stating this from page containing other info that is not related.
Good night CC.
Peace be with you !
😞
No no Casey. That is extremely relevant. Truly. You do not want to decrease NAD. You are assuming I am wrong. I’m not. I WANT to be wrong bc I want nicotine to help us but how does is effect NAD and why is that relevant?. How does it effect GABA and why is that relevant?
Someone prove me wrong and show me that lowering NAD and increasing GABA is not a problem?
Your argument is a bit like saying that glutamate has nothing to do with gluten. Not true.
Said in your style. 
Relevant? what does it mean? relevant based on what situation? and based on what dynamic context do you evaluate the relevance of something?
For example, if in a chemical reaction of a laboratory test tube you add the elements you say, you mix, you centrifuge, then you add something else you get a certain chemical result, but in the tube!
Question: What function does the test tube have and what structure does it have?
Do you understand the context?
FUNCTION AND STRUCTURE.
Can the human body have a function and structure comparable to a laboratory tube? , a good text on the anatomy of the human body will give us the theoretical answer about the differences.
Let's talk about FUNDAMENTALS
But, not enough, evaluating the relative importance of data takes a lot of practice and familiarity with using it in a proper context with honest intent and purpose.
A professional works hard and acquires practical knowledge in the field from which to evaluate the relevance of the data based on the purpose.
On the basis of these parameters I evaluate the researches.
I am only a patient, but I try to take advantage of the advice of professionals and all the observation we do through the study it's a second-hand observation and it takes a lot of practice to be a professional, that is, WORK.
I am semi-retired PwPs, don't ask me too many questions all together I don't know the answer to, please.
Relevant or not?
A warm greeting from Italy!
Gio
Nicotine decreases NAD. That IS relevant.Nicotine’s effect on GABA IS relevant.
There are costs, pros and cons, one should consider if they are considering using nicotine and those I have stated are relevant.
Gio, are you aware of the importance of NAD? And the reason for the concern about increasing GABA?
"in your style" I mean many questions in a single reply that I find overwhelming for the interlocutor who was willing to answer and nothing else. What is the first question?
My question as a former heavy smoker but who quit many years ago before Dx of PD: "What is the function of nicotine in the structure of the nervous system and why does it cause addiction?".
Here is a link titled
"Biological Mechanisms of Nicotine Addiction."
Readable, very interesting. From my personal experience as smoker (20 cigarettes a day for 26 years) I know exactly what nicotine can do for PD in practice.
Nicotine : Does it decrease NAD and increase GABA? Prompted by the original post, I entertained the idea of a nicotine patch.
So, I am digging for more info.
My hypothesis that nicotine and niacin are related was not wrong. Not the same, related. And, one has a negative effect on the other. Nicotine decreases NAD.
So, how does it effect GABA? We should be cautious with increasing GABA (I posted about this elsewhere.)
I’ve just started diving in to this but my quick look in to this leads me to presently believe that Nicotine elevates GABA.
Please jump in and please show me I’m wrong because I was really hoping for all our sakes that nicotine should be added to our arsenal.
Screen shot instead of link for brevity.
Nicotine effects GABA I was hoping nicotine patches should be added to our arsenal but given it’s effect on NAD and GABA, perhaps not a good idea?
Please dig with me to determine if nicotine can help us.
Nicotine, no thanks! Pure poison.
Perhaps in very small doses they can be neuroprotective, but they are not elements to play with.
Many years ago at my old school of agriculture and plant research center we had pure nicotine, once used as an insecticide for the cultivation of various nightshades, the lethal dose of this substance is very low and I would not recommend the use without doctor's supervision and prescription.
I have direct experience, no thanks.!
ncbi.nlm.nih.gov/pmc/articl...
However, it depends on the dosage. Alcohol is poison too. Sugar is more addictive than cocaine. And such a nicotine patch can't be more harmful than a few cigarettes a day. And it's not about the lungs! You always have to keep an eye on the side effects of the drugs against Parkinson's!
I understand, this is not a warning against smoking, but a warning commensurate with the potentially very lethal nature of PURE NICOTINE and possible misunderstandings in a public forum like this. PURE NICOTINE IS A VERY POWERFUL POISON AND THAT IS THAT!
All true and agreed. I’m considering trying a patch or maybe gum. Therefore I’ve been reading additional info on nicotine , beyond the PD info. Some of which I’ve posted. It decreases NAD. That needs to be considered. And, it’s effect on GABA needs to be clarified and considered.
For Alzheimer's, Parkinson's, psychosesNicotine as a brain booster? Why the active ingredient is not only harmful
split
It is well known that nicotine can promote diseases such as cancer. The fact that it could help against Parkinson's is less likely: in patients who were administered nicotine via patches, injections or nasal sprays, the symptoms were noticeably alleviated.
In the summer of 1926 the British Medical Journal published an article by the University of Leeds physician Henry Moll describing nicotine injections as a treatment for post-encephalitic Parkinson's disease. After inflammation of the brain tissue, those affected suffer from symptoms that are similar to the restricted mobility in Parkinson's disease. However, this usually only affects one side of the body. Although he could not have cured the patients, according to Moll, his therapeutic approach would at least alleviate their symptoms significantly. He therefore advocated further research into the method.
In the decades that followed, however, little attention was paid to the therapeutic potential of nicotine. Instead, the professional world collected more and more evidence of the massive harmful effects of cigarette smoking and the addictive potential of the alkaloid nicotine (see "The dark side of nicotine"). In 1966, the epidemiologist Harold Kahn from the National Institutes of Health was not surprised when he analyzed the medical data of almost 300,000 war veterans and the already known connection between smoking and various types of cancer as well as a shortened life expectancy was confirmed again and again. Another result of the study, on the other hand, was quite unexpected: Apparently, non-smokers develop Parkinson's three times more often than smokers. Should there be a substance in the tobacco smoke that protects those affected from the progressive degradation of the brain matter?
In fact, this question has not yet been conclusively answered. In the meantime, however, a number of findings indicate that the nicotine contained in smoke has both a protective effect and a therapeutic benefit in the disease. For example, all epidemiological studies that have been carried out on this have shown that tobacco users are less likely to develop Parkinson's disease.
In 2007, Maryka Quik of the Parkinson's Institute in Sunnyvale, California, treated squirrel monkeys with Parkinson's disease with nicotine. After eight weeks, the animals performed only half as many involuntary movements as before the start of treatment. Because of such promising results, the method was tested on individual Parkinson's patients. As a rule, they were given the substance via plasters. In fact, in many cases, the mobility impairments were reduced.
The problem: not everyone responds equally to the material. In addition, the reasons for the therapeutic effect remain unclear, which complicates the development of drugs. Laboratory experiments at least suggest that nicotine protects the brain from neurotoxins. Presumably, to some extent, it can keep certain neurons that make the neurotransmitter dopamine, which play a key role in controlling muscle movement, from dying down. In Parkinson's patients, these "dopaminergic" brain cells die off, leading to the motor deficits typical of the disease. In addition, the nicotine receptors stimulate the release of the neurotransmitter dopamine and could thus counteract the neurotransmitter deficiency caused by the disease.
Improved brain powers
The fact that nicotine can have a positive effect on the brain is now quite well documented. In 2010, a US working group led by Edward Singleton from Stevenson University in Maryland analyzed the results of 41 nicotine studies from 1994 to 2008. The subjects were given the alkaloid mostly in the form of nasal sprays, patches or injections. The evaluation showed that the substance improved fine motor skills, attention, reaction times and short-term and working memory in the short term compared to a placebo in both smokers and non-smokers. Tobacco companies were only involved in the financing of three of the studies evaluated, but this was explicitly denied in 31 studies, which speaks sufficiently for the credibility of the results.
Who funded it?
When interpreting the results of nicotine studies, it is important to note that the cigarette industry sometimes acts as a sponsor. A systematic review by Sarah Pasetes, Pamela Ling and Dorie Apollonio from the University of California in San Francisco was published in 2020. The researchers examined 32 studies on the effects of nicotine on cognition that were published between 2009 and 2016. 41 percent of the studies found a cognition-enhancing effect, 41 percent had equivocal results, and 18 percent had no effect. According to the authors, 60 percent of the studies were at least partially funded by the cigarette industry. The scientists had expected that sponsored working groups would also be more likely to report positive effects. But this was not confirmed. However, it is worrying that only one research group had made it transparent that it had received money from tobacco companies. Actually, authors have to mention a possible conflict of interest. One problem with this, however, is that there are no uniform standards in which cases it is a question of support that must be declared, write the three researchers.
Pasetes, S. et al.: Cognitive performance effects of nicotine and industry affiliation: A systematic review. Substance Abuse: Research and Treatment 14, 2020
The multiple effects of nicotine on the brain are primarily based on the fact that it activates the "cholinergic" system. These nerve cells can synthesize and release acetylcholine, one of the most important neurotransmitters in the brain. It plays a role in a wide variety of cognitive processes, as the associated receptors are found in numerous brain regions such as the hippocampus and the prefrontal cortex. In addition, acetylcholine transmits nerve impulses to the muscles at the so-called motor endplate – this is the point of contact between nerves and muscle cells.
Nicotine is also involved in the release of important messenger substances such as serotonin, glutamate, noradrenaline and, above all, dopamine. The latter is particularly crucial for the control of movement sequences as well as attention, learning and addictive behavior.
The dark side of nicotine
Nicotine is an alkaloid, a naturally occurring organic compound that has an effect on the animal or human organism. The substance occurs in the tobacco plant and other nightshade plants and serves as a defense against predators. In humans, it acts as a psychoactive neurotoxin in high doses, as it significantly disrupts the function of the autonomic nervous system. Typical symptoms include vomiting, drowsiness and an increased heart rate. It is estimated that a dose of 500 milligrams is lethal for an adult. A cigarette contains up to 13 milligrams of nicotine, but only one to three of them are absorbed by the body. When smoking, nicotine enters the bloodstream via the lungs and within ten seconds crosses the blood-brain barrier into the central nervous system. There it docks to the receptors that are actually intended for the neurotransmitter acetylcholine. One therefore also speaks of nicotinic acetylcholine receptors or nicotine receptors for short.
Among other things, the bond causes the reward center of the brain to release dopamine and a feeling of well-being and relaxation sets in almost immediately. However, regular use dulls the neural reward circuitry, so the initially small amount of nicotine needs to be increased for it to be beneficial. In addition, the brain learns that the drug is relevant to well-being; positive emotions are associated with it. These reward mechanisms are similar in all addictions and are the root cause of addiction. With nicotine there is also another addiction-promoting effect, as it improves certain brain functions. So if the next cigarette doesn't last for too long, you're unfocused and cognitively less efficient.
Dependence on tobacco products containing nicotine usually has consequences: the lungs and blood vessels in particular are damaged; the risk of a stroke, heart attack or cancer increases. There is now also evidence of a causal relationship between smoking and depression. In adolescents, smoking can also unbalance the serotonin balance and lead to anatomical changes in certain areas of the brain. According to the World Health Organization, eight million people die each year as a result of tobacco use.
The diverse mechanisms of action of nicotine apparently mean that its presence in the brain is reflected in the large neuronal networks, as a working group led by Angela Laird from Florida International University was able to show in a 2016 meta-study. The team looked at the results of 38 studies in which smokers and non-smokers were asked to either perform certain tasks or simply lie still while their brain activity was recorded using magnetic resonance imaging (MRI) or positron emission tomography (PET). According to the analysis, nicotine dampens the activity of the resting network, i.e. those brain regions that are active when doing nothing or daydreaming. At the same time, it stimulates the executive network responsible for controlled and planned actions. The authors conclude that irrelevant associations can probably be better suppressed under the influence of nicotine. At the same time, it is easier to focus on relevant external stimuli. Ultimately, this could improve attention and memory, as well as increase the speed of information processing.
"People who are on the lower performance levels and are more distractible may benefit pharmacologically from nicotine."
- Christiane Thiel, psychologist
These findings are of particular interest for medical research in connection with the fact that the number of nicotine receptors in the brain decreases with age. In a neurodegenerative disease like Alzheimer's, the loss is dramatic. Neurons of the acetylcholine system are particularly affected here, which is particularly noticeable in the cerebral cortex and hippocampus. In fact, in a study of people with mild cognitive impairments, using nicotine patches for six months ultimately resulted in better cognitive performance compared to the placebo group. According to initial indications, this could be due, among other things, to the fact that nicotine improves signal processing in those regions that are responsible for memory formation.
Nicotine can possibly help not only in neurodegenerative diseases, but also in patients with mental disorders such as schizophrenia, depression, attention deficit hyperactivity disorder (ADHD) or bipolar disorder. A striking number of those affected regularly reach for a cigarette; in schizophrenia it is almost 90 percent. All of these disorders are associated with cognitive limitations, which is why experts suspect self-medication with nicotine. This could explain why the chances of quitting are pretty poor in these patients.
Small dose, big effect
In addition to delusions, the clinical picture of schizophrenia also includes changes in sensory processing. Those affected find it difficult to ignore irrelevant environmental stimuli. Clément Dondé from the Université Grenoble Alpes concluded in a 2020 systematic review that a single dose of nicotine is sufficient to alleviate various cognitive and sensory symptoms in schizophrenia, at least in the short term. These include improvements in attention, working memory and the unconscious early recognition of stimuli. Nevertheless, the study situation is not clear as to what stands in the way of the approval of nicotine as a medicinal product.
This is where a fundamental problem becomes clear: despite decades of research and many indications of the positive effects of the alkaloid, there is only one nicotine-based drug on the market to date: a drug to stop smoking. Renowned nicotine researcher Paul Newhouse of Vanderbilt University Medical Center in Nashville cites several reasons for this. Among other things, knowledge about the correct dosage of the alkaloid is still insufficient. The role of the various molecular subunits of the nicotine receptor is also not sufficiently understood. In addition, the effect of nicotine depends heavily on the individual. Experts like Newhouse suspect that basic cognitive properties, differences in brain metabolism and the individual neuroanatomy play a decisive role in whether and how the substance affects the respective organ of thought.
Nils Richter and other researchers from the University Hospital of Cologne wanted to get to the bottom of these different modes of action. To do this, the team invited 14 patients with mild cognitive problems due to early Alzheimer's disease and healthy volunteers to a total of three sessions in which they determined the activity of various brain areas using functional magnetic resonance imaging (fMRI). In addition, memory performance tests were carried out. The participants initially received a dose of rivastigmine in the run-up to the respective measurement, the following time a placebo and finally nothing. Rivastigmine works in a similar way to nicotine; it increases acetylcholine levels and is already approved for the treatment of mild to moderate Alzheimer's dementia. As the research group points out in their 2018 publication, the drug normalized both brain activation and memory performance the most in those who initially had lower acetylcholine levels in the brain. According to the authors, it may therefore be possible to use the cholinergic system to predict the effectiveness of nicotine-based drugs.
The fact that people respond very differently to nicotine was also revealed by the test results published in 2015 by an Oldenburg working group led by psychologist Christiane Thiel. The team gave 30 non-smokers either nicotine or a placebo and then subjected them to an attention test: the participants had to press a button whenever they saw a specific target on the screen. However, other stimuli distracted from this task. It turned out that the participants who had previously received nicotine were better able to block out such disruptive stimuli. However, the effect was not the same for everyone. Rather, the nicotine effect was most pronounced in those who were normally less able to focus.
The effect of nicotine therefore apparently depends on certain basic characteristics of a person: "People who are on the lower performance level and who are more distractible can benefit pharmacologically from nicotine," says Thiel. The cognitively fitter, on the other hand, perform even worse under the influence of nicotine, as the research team was able to observe.
Who does it help?
The Oldenburgers are therefore trying to find out whether the group of people who benefit can be classified by certain characteristics. To do this, they take a close look at the individual performance level, genetic profile and brain activity of their subjects in studies. They always administer the nicotine to the participants via patch, which means that the nicotine level in the brain only rises slowly and dependence is avoided.
As early as 2015, Thomas Breckel, who was in Thiel's team at the time, discovered that special genetic variants influence the effect of nicotine on cognition. These are genes that code for acetylcholine and dopamine receptors. Breckel's colleague Stefan Ahrens was able to confirm in 2020 that the messenger substance dopamine in particular plays an important role in the effect of nicotine. After increasing the level of dopamine in the brain of some of the test subjects, he carried out a cognitive control test with them. This ability enables targeted action by hiding irrelevant information and responding flexibly to changing conditions. In contrast to the placebo group, test subjects with nicotine patches improved their cognitive flexibility – and particularly so with an increased dopamine level.
Peter Niemegeers from the University of Antwerp and his colleagues made similar observations to those of Thiel's working group. In 2014, they compared the effect of nicotine on the cognition of older subjects aged between 60 and 75 and younger subjects aged between 18 and 30. Among other things, psychomotor speed, memory and attention were tested. It turned out that in both groups, only those who did very poorly on placebo benefited. In contrast, nicotine administration impaired the performance of those who had previously done very well without the substance.
The present study results could suggest that nicotine patches are suitable as brain doping – for example when you have trouble concentrating. "I would be very reluctant to make any recommendations, because ultimately the effect depends on the starting level of the person concerned," says expert Thiel. She is critical of the entire hype surrounding "neuro-enhancement" - whether with nicotine, Ritalin or other means. "Nicotine works for some, but not for others. The use could have negative consequences, especially in young and healthy people," she says.
The Oldenburg psychologist has a different opinion when it comes to people with neuropsychiatric diseases. She sees great potential here in those whose dopamine and acetylcholine metabolism in the brain is disturbed - for example in Alzheimer's, ADHD or schizophrenia patients. According to Thiel, however, much larger study groups of 100 or 1,000 subjects would be needed. "Only then can we create an accurate profile and eventually predict who might benefit from nicotine and who might not." She hopes that on the basis of such studies it will actually be possible to develop pharmacological nicotine preparations against neuropsychiatric diseases in the future.
swell
Ahrens, S. et al.: Increased dopamine availability magnifies nicotine effects on cognitive control: A pilot study. Journal of Psychopharmacology 34, 2020
Behler, O. et al.: Nicotine reduces distraction under low perceptual load. Psychopharmacology 232, 2015
Dondé, C. et al.: The effects of acute nicotine administration on cognitive and early sensory processes in schizophrenia: A systematic review. Neuroscience and Biobehavioural Reviews 118, 2020
Heishman, S.J. et al.: Meta-analysis of the acute effects of nicotine and smoking on human performance. Psychopharmacology 210, 2010
Sutherland MT et al.: Neurobiological impact of nicotinic acetylcholine receptor agonists: An ALE meta-analysis of pharmacological neuroimaging studies. Biological Psychiatry 78, 2015
🤭 wrong place!
Nicotine affects the oral and gut biome. Very little research has been done on this. I pose the question , would using a nicotine patch be a means of avoiding possibly negative effects on our oral and gut biome while still being able to get the positive neurological effects?
Given the info thus far, I am not presently considering the gum but maybe a patch can get around the biome issue sufficiently. Again, little research to site on this.
Dr. Maryka Quik PhD. : nicotine as therapy for PD; bias and confusion against nicotine due to smoking
