23 January 2020

Quitting smoking is the best way to reduce the risk of smoking-related diseases, which include the development of certain types of cancer, cardiovascular diseases, and emphysema. Cigarette smoke also stains the teeth, causes bad breath, and ages the skin. Despite being a well-known component of tobacco, nicotine is not a primary cause of these harms. It’s many of the other harmful and potentially harmful constituents (HPHCs) in smoke that are the major cause of the health risks of smoking.

Unsurprisingly, there are many misconceptions about nicotine. How much do you really know about nicotine, and how much of that information is accurate? Read on to discover facts you may not have known about nicotine, as well as its role in tobacco harm reduction research.

A flowering tobacco plant

It starts with plants

Where does nicotine come from? The simple answer is: plants. More specifically: the Solanaceae family, commonly known as nightshade. This family includes tomatoes (~332 ng of nicotine each on average), potatoes (~675 ng), and eggplants/aubergines (~525 ng).1 To put that into perspective, a single cigarette contains ~12 mg of nicotine2 – around 18 thousand times more nicotine than a potato, by mass. But only a fraction (<2 mg) of that nicotine is transferred into the smoke of a cigarette.

What does this mean? Nicotine is present in our diet in small doses. Research estimates that people eat about 1400 ng of nicotine every day in ordinary food.2 But that doesn’t explain why tobacco and other plants contain nicotine in the first place.

Nicotine is created in the plant’s roots when two chemical compounds – pyridine and pyrrolidine – are joined together before being transported to the leaves. The genes behind this combination exists in all plants, but genetic duplications in the nightshade family are believed to have led to nicotine production.3

A tobacco leaf

Wild tobacco plants of the Nicotiana genus with higher concentrations of nicotine survived longer than sibling plants with lower concentrations.3 In other words: evolution. 

The chemical exists in these plants at greater concentrations because it benefits them. Although the primary purpose of the chemical in plants isn’t definitively known,3 studies have shown that at least one of its functions is to defend against attacking insects.4

However, nicotine’s effects in people are different from its role in plants. Since prehistorical times, people have recognized the stimulating effects of the smoke created by burning dried tobacco leaves.5 Since then, smoking has become the most common form of nicotine uptake from tobacco.

Into the brain

Commercially available products, including cigarettes, nicotine replacement therapies (NRTs), smoke-free products, and others, contain high enough levels of nicotine to temporarily affect a person’s brain function in a reversible way. But how does it get to the brain in the first place?

Nicotine from various sources can be absorbed through the lungs, through the mouth, or through the skin. The route of uptake determines the speed and intensity of nicotine delivery. Once absorbed, nicotine enters the bloodstream and is distributed, at various concentrations, to all tissues and organs, including the brain.

It takes little time after starting to use a nicotine-containing product for nicotine to reach the brain with a sufficient concentration to cause an effect. That time ranges from approximately 10 seconds as with smoking or may take an hour with the nicotine patch. Nicotine is also constantly being cleared from the body. It’s metabolized mainly by the liver, at approximately 70% with each pass through the liver, and the metabolites are excreted via the kidneys.6

The brain

Once inside the brain, nicotine binds to nicotinic acetylcholine receptors (nAChRs), such as those located on the brain’s nerve cells. These nAChRs are crucial receptors, involved in most communications between neurons in the brain but also outside the nervous system, such as between neurons and muscle cells. The natural signaling molecule for nAChRs is acetylcholine, which nicotine can imitate as it binds to these receptors. When it does, it causes the release of dopamine, GABA, glutamate, acetylcholine, and noradrenaline. As a result, nicotine may stimulate and ultimately affect short-term brain functions such as emotion, learning, and memory.

Neurons and receptors

The action of nicotine in the brain can also trigger physiological effects outside the brain. For example, the messenger epinephrine is released into the bloodstream, leading to temporary narrowing of blood vessels, higher blood pressure, and increased heart rate.

After repeated nicotine stimulation, the brain adapts to the presence of nicotine, a process that is reversible when a person stops using nicotine-containing products. This process of nicotine stimulation can ultimately lead to difficulty quitting.

This article is an excerpt of a more detailed feature from Scientific Update 8.

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