My Experience With Nicotine

Table of Contents

Nicotine is unfairly demonized because it is the active ingredient in tobacco, which is responsible for about 6 Mio. deaths per year worldwide, 25% of which are from cancer, 25% from COPD, and 50% from cardiovascular diseases. In fact, it is thought that about 30% of cancers and 90% of COPD are attributable to smoking.

Even though addictive, nicotine itself is thought to be quite safe. It is a weak stimulant and a great nootropic. It is also thought to protect against dementia, particularly Parkinson’s disease.

Personal experience

I have been using nicotine for about six years. When I first tried it, I got nauseous as this molecule was unknown to the machinery in my area postrema, a brain stem site where potentially toxic foreign stuff is detected, and nausea is generated. However, this went away completely after a couple of times.

It did not take awfully long before I was having bits and pieces of nicotine gums and lozenges multiple times per day to help with studying. I still use it frequently and perhaps this blog would not have come into existence without it.

For me, nicotine is a weak stimulant and has slight positive effects on alertness. More importantly, it has positive effects on my concentration and working memory. Nicotine is also the only stimulant I know of that can be used at night without interfering with sleep.

Furthermore, I find that nicotine is also a great self-conditioning agent. For example, if I want to read more books, I could only use nicotine when reading books. I would then probably start reading books all day.

I only ever use flavorless nicotine products. I have tried sweet and flavored nicotine products before, but I found these to be way more addictive (as sweetness itself is addictive) and also to worsen cognition.

Here and there I quit it for a couple of days, which does not result in a noticeable withdrawal. However, I consistently find myself getting back to it.

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A quick primer on cholinergic systems

Nicotine is a cholinergic drug. There are various cholinergic transmitter systems in the human brain. Acetylcholine is sort of an “activity-amplifier” in many cortical and subcortical brain networks. One important cholinergic nucleus is the nucleus basalis (NB) in the forebrain. This nucleus supplies a variety of cortical areas with acetylcholine, amplifying their activity, particularly some areas in the prefrontal cortex.

Drugs that block cholinergic receptors, such as antipsychotics or tricyclics, are essentially “dumb drugs” and they are also associated with cognitive impairment and dementia.

Conversely, drugs that increase levels of acetylcholine, such as cholinesterase inhibitors, are often employed for the symptomatic treatment of dementia and are used off-label to induce lucid dreaming. Nicotine itself reliably enhances cognitive performance on a whole range of tests.

Alpha-GPC or CDP-choline, both of which are choline precursors, also work via stimulating cholinergic systems. I have tried alpha-GPC a couple of times and I find it useful when I am sleep-deprived.

I supplement with 2400mg of phosphatidylcholine per day. I discuss the supplements I take (and why I take them) in more detail here.

How it works

Nicotine exerts its effects through the agonism (activation) of various receptors of the nicotinic type (which were named after nicotine), resulting in multiple downstream effects. I will only discuss its nootropic effects, and not its effects on the autonomic nervous system, basal ganglia systems, or brain stem activity.

There are three main reasons why nicotine is a nootropic:

  • The nucleus basalis has cholinergic projections to various cortical areas, where acetylcholine amplifies the activity of certain networks, thereby making them “sharper”. Cholinergic projections are particularly dense to the dorsolateral prefrontal cortex, which is important for selective attention and other executive functions, and the hippocampus, which is important for memory formation.

  • Acetylcholine signaling increases dopamine release, which increases motivation, mood, and focus. This is also the reason behind nicotine being so habit-forming.

  • Nicotinic receptors are found in the sympathetic pre-ganglia of the sympathetic nervous system. Nicotine’s activation of these receptors increases sympathetic nervous system activity. Among other things, this also increases the tonic release of adrenaline. Adrenaline then acts on the vagus nerve, which transmits to the reticular activating system, and in turn, increases brain noradrenaline levels, which helps with alertness, attention, and focus. Noradrenaline is discussed in more detail in An Introduction to Neurotransmitters.

Together, these effects (acetylcholine; dopamine; adrenaline) cause nicotine to be a powerful nootropic without being too much of a stimulant.

At low doses, nicotine has both relaxing and stimulating properties. However, at higher doses, nicotine’s effects on the parasympathetic nervous system become predominant and it has mostly relaxing and sedating properties.

Nicotine and weight loss

Smokers consistently weigh less. Many assume that this is because nicotine has appetite-suppressant effects, though this is not the whole story.

The nicotine-induced increase in area-under-curve levels of adrenaline significantly increases basal metabolic rate (BMR), and heavy smokers burn about 300-500kcal more per day. Thus, the weight gain associated with smoking cessation is not only due to increased caloric intake but also due to decreased energy expenditure.

I estimate that my use of nicotine has me burn about 150-250 kcal more per day. I discuss BMR in more detail here.

Addiction potential

Nicotine is addictive and setting oneself up for a potentially life-long addiction and cravings is not to be taken lightly, even if the health effects of nicotine itself are far below those of smoking cigarettes (which is a low bar to meet).

Nicotine is unique in that it is addictive without causing much euphoria. However, its addictiveness depends somewhat on the way it is administered.

For example, smoking a single cigarette causes about 2mg of nicotine to be absorbed within a few minutes, with well-marked “hits” every couple of seconds. Conversely, with a bioavailability of 50-60%, a 2mg nicotine lozenge delivers about 1mg of nicotine over 30 minutes and in a much more sustained fashion.

As is the case with other substances, the faster and greater the plasma peak, the more addictive the substance. Conversely, the slower the peak, the lower the dopamine spike, the lower the addictiveness.

Therefore, slowly absorbing delivery vehicles have a reduced addictiveness (gum & lozenge >> snus >> smoking & vaping). Furthermore, I prefer flavorless products because an ongoing pleasure reaction, such as due to having something sweet in one’s mouth, decreases executive functions for evolutionarily obvious reasons (“Dear animal do not think too much and keep doing whatever you are doing!”).

Some researchers claim that tobacco products contain molecules with MAO inhibiting properties, which supposedly enhance nicotine’s addictiveness even further. This is probably bullshit (at least in vivo). If this were the case, then any stimulant or serotonergic molecule floating around in a smoker’s body at the time of nicotine consumption would be strongly potentiated. Given that a lot of smokers are on stimulants or antidepressants, this does not seem to be the case. MAO inhibitors are discussed here.

The addiction potential of the different ways of nicotine consumption

In descending order:

  • Vaping: Because there is no inhalation of tobacco’s shitty combustive byproducts, vaping is presumably less detrimental to health. However, the addiction potential is even greater than that of cigarettes because blood nicotine levels reach higher peaks, in part due to greater nicotine content, and in part due to the combustion mechanism of the delivery vehicle itself.

  • Cigarettes: When nicotine is smoked, nicotine is delivered in a “puff”-fashion, which causes dopamine micro-spikes. Furthermore, the activity of smoking itself, coupled with the dopamine microspikes that happen during the activity of smoking, is addictive. Smokers are basically conditioning themselves to engage in the activity (incl. environment) of smoking in the same way coffee drinkers are conditioning themselves to engage in the activity (incl. environment) of drinking coffee.

  • Snus: Because absorption through the buccal mucosa is slower than through the lungs, consuming nicotine in the form of snus/pouch does not result in a sharp rise in nicotine plasma levels, and therefore dopamine levels. However, the nicotine absorbed by a single pouch is thought to be on the order of 10mg, which is five times as much compared to a cigarette. This makes snus highly addictive.

  • Gum/lozenge: The way I consume nicotine (e.g., one 4mg gum over two hours) gives me about as much nicotine over two hours as a cigarette would over 5 minutes. While addictiveness is definitely not absent, the comparatively low nicotine content and especially the drawn-out plasma curve make gum/lozenge less addictive than other forms of nicotine administration.

  • Patch: Nicotine patch has obviously the lowest addictiveness, though one loses the ability to use nicotine selectively for certain activities.

Other experience reports

For a discussion of the molecular correlates of well-being, and links to accounts of various related molecules I have experimented with, read here.

For a full list of experience reports click here.

Sources & further information

Disclaimer

The content available on this website is based on the author’s individual research, opinions, and personal experiences. It is intended solely for informational and entertainment purposes and does not constitute medical advice. The author does not endorse the use of supplements, pharmaceutical drugs, or hormones without the direct oversight of a qualified physician. People should never disregard professional medical advice or delay in seeking it because of something they have read on the internet.