TIME FOR THE SCIENCE THAT PROVES
WHY PSEUDOSMOKING WORKS SO WELL and why
Pseudosmoking is only applicable to cigarette smokers.
The number one thing you do when you begin your trials to quit smoking is you build yourself up to quit by physically and "symbolically" throwing away your remaining cigarettes, so you don't have access to them anymore. AND so it begins. Within hours of smoking your "last" cigarette, the withdrawal begins. Ahaaaaa, but you were prepared and have every known nicotine replacement aid readily available, You began with 2 patches, (just to be sure) but its not really helping. Ahaaaa, but you were prepared with snacks to help you get by too, but they aren't really helping either. Ahaaaaaa, but you have a selection of books and dvd's to watch to take your mind off the cravings, not cutting it. Ahaaaaaa, but you have interesting projects to undertake to ease your building ANXIETIES. Not WORKINGGGGGGGGGG?...and then you went to a quitsmoking forum where they were patronizing in the extreme....NOT HELPING....There is a reason. You threw away THE best available quit smoking aid before you started. YES, your cigarettes. Here's why I have the temerity to say so.
The thing is, What ALL quit smoking methods do, (including Pseudosmoking), effective long term or not, is stop nicotine getting to your lungs. What almost all, (NOT PSEUDOSMOKING) established methods ONLY do is try and treat the symptoms of withdrawal with nicotine replacement therapies or other drugs. The very real, but MASSIVELY under rated situational issues also confronting the quitting smoker, for a much LONGER period of time are treated with a there, there, you can do it, you have managed 2 hours already, slap on another patch and try twiddling your thumbs faster, approach. How anyone quits smoking at all those ways? Hats off to you, wow...I couldn't .....PseudoSmoking is the ONLY method that addresses EVERY issue easily and effectively with the quitting smoker able, for the most part, to carry on life as if not much had changed. What ABSOLUTELY FLOORS ME is it has taken this long to be figured out.
This website goes into quite good detail about my conclusions why continuing to use cigarettes to quit smoking is a good idea as long as they are PseudoSmoked. What it doesn't do is have any proof other than my own conclusions and educated guesses from my experiences in actually quitting doing so. Also why there are no references to publications or other media to support my claims as I didn't use any. Personal experience only. To date science has proven me pretty well on the mark aside from one area which is nrt's.
This is because there are 2 mechanisms in the brain dealing with nicotine. The major one deals with lung absorbed "fast nicotine" eg inhaled which MUST be eliminated quickly and IS by all methods. The other skin or oral cavity absorbed "slow" nicotine, that nrt's work by and oral absorption of the nicotine in the cigarette smoke in the PseudoSmoking method. I am still against over the counter nrt products as they are prone to lack of use, over use and don't deal adequately with the cravings of situational habit which is the major cause of relapse.
Think of it this way, I love analogies, having ANY sexual experience with someone you care a great deal about (The smoking a cigarette experience ) is infinitely more satisfying than masturbation ( cold turkey, NRT's or the prescription medications ). Can you see why PseudoSmoking to quit smoking leaves the other methods in its tracks?
That is what this page is about for those that NEED the science behind the theory. ENJOY
I am not going to do what most do and cut and paste all they want you to read and none of what they would prefer you didn't, just in case you have a brain and can work out they're actually trying it on....just a bit. I will copy one complete body of text from a document that sums most of it up in one effort, another an exerpt of the relevant section from within a pdf document. I am then going to give my own unqualified overall summary of the reports of scientific studies into the why's and wherefors about nicotine addiction and related issues AND provide outside links to these studies and others over time for checks and balances.
Here goes. This is using the assumption that the PseudoSmoking "fast (LUNG ABSORBED) nicotine" weaning process has been completed satisfactorily and you are 100% PseudoSmoking.
By PseudoSmoking you prevent the possibility of inhaling cigarette smoke and therefore nicotine down into your lungs simply because your lungs are already close to capacity before you even take a drag of your cigarette. Ok, all methods are now equal in this regard as they all do this, (no smoke inhaled into lungs) the others just don't let you smoke at all.
With PseudoSmoking you draw the cigarette smoke into your mouth, but it can not go further ( or you're doing it wrong, simple) ITS WHY IT WORKS. You hold it there for a few seconds and then exhale. Only a few % of the total cigarette smoke holds nicotine. Due to cigarette smokes acidity, due to heat curing of the tobacco, ( done as it reduces irritation and therefore coughing) only a minute percentage of this this already very low nicotine percentage of total smoke volume, passes through the mucous membranes within the mouth and into the bloodstream. This takes time.
This is exactly what your oral nicotine replacement therapy aids do, but for longer periods or continuously via patches and generally at a higher dose than the total oral nicotine absorption from the cigarette smoke only. I'll do the maths one day too. Both the gum and lozenges have the nicotine contained in an alkaline medium which very readily passes through the mucous membranes of the mouth. Also why PseudoSmoking is NOT suitable for cigar smokers due to a cigar tobacco's naturally dried alkalinity. Do not confuse any graphs that contain inhaled nicotine from cigarette smoke with any that are orally held cigarette smoke only,
Most graphs will not show cigarette smoke only derived nicotine absorption by the mucous membranes, as the take up of nicotine in this manner is very, very small (inhaled will show as a sharp rise and quite rapid fall, a spike, where orally held is low take up and stays moderately flat). Where PseudoSmoking is without peer is in the situational issues where ALL other methods either don't address, can't address or don't bother about.
PseudoSmoking deals with this easily as NOTHING much has changed. There is no stress, there is no anxiety there is no pressure. You PseudoSmoke, you have no fast nicotine addiction, you smoke less and less as a matter of course due to continued lower nicotine levels AND as you address all the nicotine web strand triggers, you stop smoking when you feel comfortable to do so. Read the research, the rest, which is simple common sense, is well covered within this website and doesn't need scientific clarification. If you believe otherwise, please let me know.
Please be advised that any cancer risks from any form of smoking are well covered elsewhere and are also widely known. The media and anti cancer groups have been very useful for this. Just in case people aren't aware, cigarette smoke is proven to cause various cancers. By continuing to smoke in any manner, including PseudoSmoking up until you quit, you acknowledge and personally accept the possible consequences of those risks. I accept and recognize that fact throughout my web pages. End of discussion.
The point of the exerise is for people to be able to quit smoking. As quitting is deemed difficult, many people delay doing so until an event occurs that spurs them into wanting to quit. This may be many years down the track and therefore compounds the perceived and very real problem with quitting. With most current methods it remains a difficult process and is open to multiple failure events and having to try again at a later stage. Is it any wonder people don't want to even try to quit smoking??? Does it have to be this hard? No. Pseudosmoking removes this difficulty and if done correctly ( it should be, its extraordinarily easy to do) should allow the smoker to easily quit smoking in one effort.
Cigarette smoking is a complex behavior that becomes powerfully conditioned by several types of biobehavioral mechanisms. To use a metaphor, the nicotine-addicted cigarette smoker may be viewed as a person held by many chains, some of which hold much more strongly than others. For some people, eliminating one or two of the chains is sufficient for them to break the addiction. This metaphor could be taken more lightly except for the fact that of the nearly 20 million people who attempt to quit smoking each year, less than 7% remain abstinent for a year; of those who do remain abstinent for a year, nearly 1/3 relapse thereafter!( 1)
That's scary stuff indeed and another reason why PseudoSmoking NEEDS to be known about. Current methods are not good enough. It is understood that nicotine isn't the only issue to this dilemma, as even with adequate nicotine in the system from other sources, cravings still occur which is not understood and ergo relapses.
My method of PseudoSmoking achieves the required elimination of nicotine reaching the lungs. A planned reduction over approx 3 weeks of nicotine reaching the lungs again helps as it is not an abrupt stoppage of nicotine absorption by the lungs. Thereafter PseudoSmoking otherwise interfers very little in the daily habits, rituals, external and sensual experiences involved with smoking cigarettes from which I believe the cravings stem from and fail to be addressed.
By leaving the basic smoking experience intact for any given situational triggers, the reduced nicotine uptake,( plenty of reading below explains why) due to the method of Pseudosmoking appears to be accepted by the brain as nothing abrupt is changing, especially as you make a choice, to Pseudosmoke in this instance or not. This leads to the need to smoke in those same situations being reduced over time to such a point where no dependant or habitual reason exists to continue smoking and the smoker can simply stop when they wish to. Just as I did.
I often harp on about the importance of the situational habit, it IS yet another reason PseudoSmoking should be the quitters choice.
Ferguson SG, Shiffman S. The relevance and treatment of cue-induced cravings in tobacco dependence. J Subst Abuse Treat 2009;36:235–43.
Craving to smoke is often conceptualized and measured as a tonic, slowly changing state induced by abstinence. In this article, we review the literature on the existence, causes, and treatment of cue-induced cravings: intense, episodic cravings typically provoked by situational cues associated with drug use. In laboratory research, smokers exposed to smoking-related cues demonstrate increased craving as well as distinct patterns of brain activation. Observational field studies indicate that such cue-induced cravings are substantially responsible for relapse to smoking but that smoking can often be averted by coping responses. The effects of pharmacological interventions are mixed. Steady-state medications (bupropion, varenicline, nicotine patch) do not appear to protect smokers from cue-induced cravings. However, acutely administered nicotine medications (such as nicotine gum and lozenge), used after cue exposure as "rescue medications," can help a smoker's recovery from cue-inducedcravings. Cue-induced craving plays an important role in smoking and relapse and likely in other addictions as well. Treatments to mitigate the effect of cue-induced craving are both important and needed.
This simply means that when a situational event happens it needs to be attended to. Pseudosmoking gives the nrt effect every cigarette you PseudoSmoke. With PseudoSmoking you do get to choose though whether to light up or not. The point is YOU CAN. One thing we know is we never go ANYWHERE without our smokes or run out. As is stated above nicotine patches don't cut it here and lozenges and gum or sprays might, (There IS a use for a MAN BAG), but you may not have them with you, you may have run out. They simply may not give you all of the entire experience of the ritual of smoking your brain requires in that instance on top of the nicotine to prevent the cravings.
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.The nicotinic cholinergic receptor consists of five subunits.
The brain expresses nine α subunits (α2 through α10) and three β subunits (β2 through β4). The most abundant receptors are α4β2, α3β4, and α7, the latter of which are homomeric.
The α4β2* is the principal mediator of nicotine dependence.
In mice, disruption of the β2 subunit gene eliminates the behavioral effects of nicotine; reinserting the gene into the ventral tegmental area restores behavioral responses to nicotine.
The α4 subunit is an important determinant of sensitivity to nicotine.
A mutation affecting a single nucleotide in the receptor gene increases the hypersensitivity to the effects of nicotine.
The presence of α5 subunit combined with α4β2 increases calcium conductance seven times; α5 gene variants also alter nicotine responsiveness in cultured human cells.
Theα3β4 subtype probably mediates the cardiovascular effects of nicotine.
The α7 homomeric receptors are involved in rapid synaptic transmission and long-term potentiation to dopaminergic neurons at excitatory inputs and have a role in learning and sensory gating.
Smoke particles carry the nicotine into the lungs, where it is rapidly absorbed into the pulmonary venous circulation. The nicotine then enters the arterial circulation and moves quickly from the lungs to the brain, where it binds to nicotine cholinergic receptors (ligand-gated ion channels that normally bind acetylcholine).
The binding of nicotine between two subunits of the receptor opens the channel, allowing the entry of sodium or calcium.
The entry of these cations into the cell further activates voltage-dependent calcium channels, allowing more calcium to enter.
One of the effects of the entry of calcium into a neuron is the release of neurotransmitters.
Nicotine and Neurotransmitter Release
Stimulation of nicotinic cholinergic receptors releases a variety of neurotransmitters in the brain.
One of them, dopamine, signals a pleasurable experience and is critical for the reinforcing effects (effects that promote self-administration)of nicotine and other drugs of abuse.
Experimentally induced lesions in dopamine-releasing neurons prevent self-administration of nicotine in rats.
Nicotine releases dopamine in the Mesolimbic area, the corpus striatum, and the frontal cortex.
The dopaminergic neurons in the ventral tegmental area of the midbrain and in the shell of the nucleus accumbens are critical in drug-induced reward (both regions have a role in perceptions of pleasure and reward).
Nicotine also augments both glutamate release, which facilitates the release of dopamine, and γ-aminobutyric acid (GABA) release, which inhibits dopamine release.
With long-term exposure to nicotine, some nicotinic cholinergic receptors become desensitized but some do not.
As a result, GABA-mediated inhibitory tone diminishes while glutamate-mediated excitation persists, increasing excitation of dopaminergic neurons and enhancing responsiveness to nicotine.
Nicotine lowers the threshold for electrical stimulation in reward system, leading to increased responsiveness to rewarding stimuli an effect that can last for more than 30 days.
It also increases activity in the prefrontal cortex, thalamus, and visual system, reflecting activation of the reward network), and releases dopamine in the striatum.
Other neurotransmitters that may be involved in nicotine addiction are the hypocretins, neuropeptides produced in the lateral hypothalamus that regulate the stimulatory effects of nicotine on reward centers in the brain and modulate self-administration of nicotine in rodents.
The Biology of Nicotine Addiction
Nicotine acts on nicotinic cholinergic receptors, triggering the release of neurotransmitters that produce psychoactive effects that are rewarding.
With repeated exposure, tolerance develops to many of the effects of nicotine, reducing its primary reinforcing effects and inducing physical dependence (i.e., withdrawal symptoms in the absence of nicotine).
Smoking behavior is influenced by pharmacologic feedback and by environmental factors such as smoking cues, friends who smoke, stress, and product advertising.
Levels of nicotine in the body in relation to a particular level of nicotine intake from smoking are modulated by the rate of nicotine metabolism, which occurs in the liver largely by means of the enzyme CYP2A6.
Other factors that influence smoking behavior include age, sex, genetics, mental illness, and substance abuse.
With repeated exposure to nicotine, neuroadaptation (tolerance) to some of the effects of nicotine develops
As neuroadaptation develops… the number of binding sites on the nicotinic cholinergic receptors in the brain increases, probably in response to nicotine-mediated desensitization of receptors.
Desensitization — ligand-induced closure and unresponsiveness of the receptor —is believed to play a role in tolerance and dependence: the symptoms of craving and withdrawal begin in smokers when desensitized α4 β2* nicotinic cholinergic receptors become responsive during periods of abstinence, such as nighttime sleep.
Nicotine binding of these receptors during smoking alleviates craving and withdrawal.
Cigarette smoking maintains near-complete saturation — and thus desensitization — of theα4 β2* nicotinic cholinergic receptors.
Thus, smokers are probably attempting to avoid withdrawal symptoms when maintaining a desensitized state By sustaining sufficient levels of plasma nicotine to prevent withdrawal symptoms, they also derive rewarding effects from the conditioned reinforcements associated with smoking, such as the taste and feel of smoke.
Nicotine withdrawal causes anxiety and stress, both of which are powerful incentives to take up smoking again.
The negative affect that typifies the response to nicotine withdrawal probably results in part from a cascade of events involving increased levels of extra hypothalamic corticotrophin-releasing factor (CRF) and increased binding of CRF to corticotropin-releasing factor 1 (CRF1) receptors in the brain, thereby activating the CRF–CRF1 receptor system, which mediates responses to stress.
Anxiety-like behavior and the release of CRF in the central nucleus of the amygdala occur during nicotine withdrawal.
CRF causes anxiety, whereas the pharmacologic blockade of CRF1 receptors inhibits the anxiogenic effects of nicotine withdrawal. The blockade of CRF1 receptors also prevents the increase in self-administration of nicotine that occurs during abstinence from nicotine.
Thus, both underactivity of the dopaminergic system and activation of the CRF–CRF1receptor system contribute to the symptoms of nicotine withdrawal that often precipitate relapse.
Clinical Aspects of Nicotine Addiction
Psychoactive Effects of Nicotine
Nicotine induces pleasure and reduces stress and anxiety. Smokers use it to modulate levels of arousal and to control mood. Smoking improves concentration, reaction time, and performance of certain tasks.
Relief from withdrawal symptoms is probably the primary reason for this enhanced performance and heightened mood.
Cessation of smoking causes the emergence of withdrawal symptoms: irritability, depressed mood, restlessness, and anxiety.
The intensity of these mood disturbances is similar to that found in psychiatric outpatients.
Anhedonia — the feeling that there's little pleasure in life — can also occur with withdrawal from nicotine, and from other drugs of abuse.
The basis of nicotine addiction is a combination of positive reinforcements, including enhancement of mood and avoidance of withdrawal symptoms.
In addition, conditioning has an important role in the development of tobacco addiction.
When a person who is addicted to nicotine stops smoking, the urge to resume is recurrent and persists long after withdrawal symptoms dissipate.
With regular smoking, the smoker comes to associate specific moods, situations, or environmental factors — smoking-related cues —with the rewarding effects of nicotine. Typically, these cues trigger relapse.
The association between such cues and the anticipated effects of nicotine, and the resulting urge to use nicotine, constitute a form of conditioning.
Studies show that nicotine exposure causes changes in the protein expression of brain cells and in their synaptic connections— a process termed neural plasticity —which underlie conditioning. Nicotine also enhances behavioral responses to conditioned stimuli, which may contribute to compulsive smoking.
The desire to smoke is maintained, in part, by such conditioning. Smokers usually take a cigarette after a meal, with a cup of coffee or an alcoholic drink, or with friends who smoke, when repeated many times; such situations become a powerful cue for the urge to smoke
Aspects of smoking itself — the manipulation of smoking materials, or the taste, smell, or feel of smoke in the throat — also become associated with the pleasurable effects of smoking. Even unpleasant moods can become conditioned cues for smoking: a smoker may learn that not having a cigarette provokes irritability and that smoking one provides relief. After repeated experiences like this, a smoker can sense irritability from any source as a cue for smoking.
Functional imaging studies have shown that exposure to drug-associated cues activates cortical regions of the brain, including the insula. Smokers who sustain damage to the insula (e.g., brain trauma) are more likely to quit smoking soon after the injury, and to remain abstinent, and are less likely to have conscious urges to smoke than smokers with brain injury that does not affect
The Tobacco Addiction Cycle
The first cigarette of the day has a substantial pharmacologic effect, primarily arousal, but at the same time, tolerance to nicotine begins to develop
A second cigarette is smoked later, at a time when the smoker has learned
That there is some regression of tolerance. With subsequent smoking, there is an accumulation of nicotine in the body, resulting in a greater level of tolerance, and withdrawal symptoms become more pronounced between successive cigarettes. Transiently high levels of nicotine in the brain after individual cigarettes are smoked may partially overcome tolerance, but the primary (euphoric) effects of nicotine tend to lessen throughout the day.
Abstinence overnight allows considerable resensitization to the actions of nicotine.
Genetics of Nicotine Addiction
Studies in twins have shown a high degree of heritability of cigarette smoking (≥50%), including the level of dependence and the number of cigarettes smoked daily. these studies have also revealed the heritability of the particular symptoms that occur when a smoker stops smoking.
Numerous attempts have been made to identify genes underlying nicotine addiction.
Candidate genes coding for nicotine receptor subtypes, dopamine receptors and dopamine transporters, GABA receptors, opiate and cannabinoids receptors, and other types of receptors have been associated with different aspects of smoking behavior.
Vulnerability to Addiction
Tobacco use typically begins in childhood or adolescence— 80% of smokers begin smoking by 18years of age. Although two thirds of young people try cigarette smoking, only 20 to 25% of them become dependent daily smokers, usually as adults.
Risk factors for smoking in childhood or adolescence include peer and parental influences, behavioral problems (e.g., poor school performance), personality characteristics (rebelliousness, risk taking, depression, and anxiety), and genetic influences.
The risk of dependence increases when smoking begins early. Studies animals suggest that nicotine can induce permanent changes that lead to addiction. Brain changes in adolescent rats exposed to nicotine are greater than those in exposed adult rats.
Adolescent rats that have been exposed to nicotine have higher rates of nicotine self-administration as adults, which is consistent with the idea that early exposure to nicotine increases the severity of dependence.
Tobacco addiction is highly prevalent among persons with mental illness or substance-abuse disorders. The mechanisms of this association are likely to include a shared genetic predisposition, the capacity of nicotine to alleviate some psychiatric symptoms, and the inhibitory effects of tobacco smoke on monoamine oxidase.
Smoking behavior in women is more strongly influenced by conditioned cues and negative affect; men are more likely to smoke in response to pharmacologic cues, regulating their intake of nicotine more precisely than women.
On average, women metabolize nicotine more quickly than men, which may contribute to their increased susceptibility to nicotine addiction and may help to explain why, among smokers, it is more difficult for women to quit. those who metabolize nicotine rapidly take in more cigarette smoke per day than those who metabolize nicotine slowly. Nicotine is metabolized to cotinine primarily by the liver enzymes.
Persons with a genetic basis for slow metabolism smoke fewer cigarettes daily than persons with faster metabolism.
Rapid metabolism of nicotine is associated with more severe withdrawal symptoms and a lower probability of success in quitting during nicotine-patch treatment.
Nicotine sustains tobacco addiction, a major cause of disability and premature death, by acting on nicotinic cholinergic receptors in the brain to trigger the release of dopamine and other neurotransmitters.
Release of dopamine, glutamate, and GABA is particularly important in the development of nicotine dependence, and CRF may play a key role in withdrawal. Neuroadaptation and tolerance involve changes in nicotinic receptors and neural plasticity. Nicotine addiction occurs when smokers come to rely on smoking to modulate mood and arousal, relieve withdrawal symptoms, or both. Light smokers smoke mainly for positive reinforcement in specific situations. Genetic studies indicate that nicotinic receptor subtypes and the genes involved in neuroplasticity and learning play a part in the development of dependence.
People with psychiatric or substance-abuse disorders, who account for a large proportion of current smokers, have an increased susceptibility to tobacco addiction. Nicotine is metabolized in liver, and variation in the rate of nicotine metabolism contributes to differences in vulnerability to tobacco dependence and the response to smoking-cessation treatment.
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The most abused drug, along with alcohol, is nicotine. It is a plant derived substance. A single cigarette has very little nicotine - 95% of the cigarette smoke is volatile matter (nitrogen, carbon monoxide, benzene, hydrogen cyanide, all the nasty things that cause cancer). Nicotine (5% of the particulate smoke) is an alkaloid which is contained within tar droplets, which are very lipid soluble and pass down into the lungs and onto the bloodstream.
Pharmacokinetics There are numerous ways of administering nicotine. Nicotine spray (intranasal) contains about 1mg of nicotine (20-50% gets into the bloodstream). Nicotine gum contains 2 to 4mg of nicotine (50-70% gets into the bloodstream). Cigarettes contain about 9-17mg of nicotine (only about 20% gets into the bloodstream). Nicotine patches contain about 15 to 22mg which are applied over 24 hours (70% gets into the bloodstream transdermally).
Nicotine itself has a pKa of about 7.9, and cigarette smoke is relatively acidic. So most of the nicotine in smoke is actually ionised, which means very little nicotine gets from the smoke into the bloodstream via the mucous membranes of the mouth - nearly all of it is absorbed in the lungs, because the alveoli are so thin it doesn’t matter if its ionised. The spray, gum and patch are buffered to make them as close to the pKa of nicotine as possible so that the nicotine is absorbed as much as possible.
The cigarette is clearly the quickest route of administration - very high levels achieved very quickly. The spray is also quite rapid. Oral administration always shows the slight delay, and the patch has very low levels over a long time. With the spray, gum and patch, the aim is to remove the nicotine “spike”, which tends to encourage the individual to take another cigarette. To wean people off cigarettes, you want a low level of nicotine over a long period of time.
The half life of nicotine is a couple of hours. It is broken down predominantly (70-80%) in the liver by hepatic cytochrome P2A6 into cotinine, and this is excreted in the urine. The relatively quick clearance is why there is repetitive abuse of the drug.
Pharmacodynamics Nicotine acts on nicotinic acetylcholine receptors in the autonomic nervous system. There are five subunits that make up the receptor.
The most important are the CNS nicotinic acetylcholine receptors. Generally speaking, α4 and β2 subunits are what nicotine binds to in order to produce the effects.
Like cocaine, nicotine has quite a direct effect in terms of euphoria. Nicotine binds to the nicotinic acetylcholine receptors on cell bodies of dopaminergic neurons in the ventral tegmental area. This stimulates them and activates them to release dopamine into the nucleus accumbens.
This is a less potent effect than that achieved with cocaine in terms of producing euphoria. The euphoric effect wears off during the day.
The main side effects of nicotine are cardiovascular effects. Cancer and cardiovascular disease are associated with smoking, but only the cardiovascular effects are due to nicotine itself. Nicotinic ACh receptors are present Sybghat Rahim 35 throughout the autonomic nervous system. The CVS effects are increased heart rate and stroke volume, profound vasoconstriction (particularly in the coronary arterioles and the skin), which leads to blood flow problems in these tissues. There is also vasodilation in skeletal muscle. Increased lipolysis is also caused by nicotine, which worsens the lipid profile in the blood (free fatty acids, VLDLs, low HDL levels). Nicotine also increases platelet activity because of enhanced thromboxane A2, and reduced nitric oxide. All of this together, combined with the fact that the heart is working harder than it should, the blood flow to the heart is reduced, and the likelihood those vessels will get blocked is why cardiovascular risks are so strong.
Metabolic effects of nicotine are that it increases metabolic rate, and it is also an appetite suppressant. Looking at a study where individuals who stopped smoking were followed for two years, there was between a 6.7 to 9.8% weight gain.
There is evidence that nicotine actually protects against Parkinson’s disease, as it increases brain cytochrome P450, which metabolise a lot of neurotoxins in the brain. It is also protective against Alzheimer’s disease, as nicotine decreases β-amyloid toxicity and the build up of amyloid precursor proteins (APP).
Summary Nicotine is derived from the plant Nicotana tabacum. In cigarettes, nicotine is 5% of the particulate matter. It’s onset is within a matter of seconds, and it has a tissue half life of between 2 to 3 hours. Its elimination is by converting it to cotinine in the liver (70-80%). It works in the body by activating nicotinic acetylcholine receptors to produce euphoria. It also increases metabolic rate and suppresses appetite, but there are strong links with cardiovascular disease. There are some protective effects against Parkinson’s disease and Alzheimer’s disease.
More relevant websites and reading for you.
How much more would you like to know?
So in essence, all of the above says in order to quit smoking, you NEED to get rid of any nicotine element as much as possible and my method of PseudoSmoking enables this easily and almost withdrawal free, if the smoke can't reach your lungs.......jobs done. It also enables you to rid yourselves of the situational habit very easily over time, which is almost 95% of the reason most people FAIL to quit smoking permanently the first few times they try cold turkey. Its not the nicotine withdrawal, with my method that's done and dusted in a week or 2 if you even notice it at all, its the unconscious habit all smokers have when in situations they would normally smoke, when relapses happen. Don't put yourself through all of that. PseudoSmoking makes even this a doddle.
PseudoSmoke to easily quit smoking, once only and for good
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