Wine and cigarettes

Legally sound?

If something’s legal, does that mean it’s safe?

Tobacco

When you smoke, what are you actually breathing in? Cigarette smoke contains over 7,000 chemicals, including at least 60 cancer-causing substances (carcinogens). One of the most dangerous components, tar, which is produced by burning tobacco, is the main cause of lung, mouth and throat cancer in smokers. When breathed in, it destroys the cilia, fine hairs in the upper airway that protect against infection. Once the cilia are damaged, the tar can then move further into the lungs, causing coughing and shortness of breath.

This damage can lead to emphysema, a disease of the lungs that weakens the bronchioles (small airways in the lungs) and alveoli (small sac-like structures). This can lead the alveoli to rupture, creating a larger air space rather than many small ones, which reduces the surface area of the lungs. This makes the lungs less efficient at transferring oxygen into the blood and transferring carbon dioxide from the blood to the lungs’ air space.

The other well-known component of cigarettes is nicotine. Nicotine is absorbed through the skin and the mucosal lining (lining of passages that are in contact with the air) of the nose, mouth and lungs, and rapidly peaks in the bloodstream and brain. It can reach the brain just 10 seconds after inhalation. Nicotine itself isn’t thought to be much worse for you than caffeine – but both do cause a short-term increase in blood pressure and pulse rate, which could affect your health.

In the brain, nicotine mimics acetylcholine, a neurotransmitter involved in muscle movement, alertness, learning and memory. Nicotine also interacts with the dopamine reward pathway (see our article on the brain’s reward system), and is the chemical that makes people addicted to smoking.

More recently, nicotine has also been shown to be associated with a lower rate of Parkinson’s disease – with studies showing that people with Parkinson’s were less likely to have been smokers than the rest of the population. Nicotine binds to receptors in an area of the brain called the striatum, which is located near the areas that regulate and emit dopamine – the neurotransmitter that is deficient in Parkinson’s disease.

It has been suggested that nicotine could be used medically to stimulate nerve cells to boost dopamine levels. Research in animal models of Parkinson’s disease has shown that nicotine administration reduces tremors. This suggests a possible new use of nicotine when removed from the harmful context of tobacco.

Alcohol

Many people associate alcohol with slurred speech and impaired judgement, but how does it cause these effects? The alcohol someone drinks is actually ethanol, and it enters the bloodstream through the stomach and small intestine through digestion, before being transported to the brain. Here it acts as a depressant – even though most of us will associate alcohol intake with increased energy. In the brain, alcohol increases the amount of GABA (gamma-aminobutyric acid), an inhibitory neurotransmitter, and decreases glutamate, an excitatory neurotransmitter. This produces a range of effects, including lowering of inhibitions and slowing of thought, speech and movement.

Alcohol also acts to increase dopamine, but probably not in the same way as nicotine or other drugs. It is thought that alcohol’s effect on GABA can have a knock-on effect on dopamine release or production, creating a pleasurable feeling – which may lead to addiction.

As well as these short-term effects, alcohol can cause a range of long-term effects, especially if consumption begins in adolescence, before the brain has fully developed. Brain-imaging studies of people who began drinking alcohol during adolescence has suggested that this can cause structural and functional abnormalities in a part of the brain called the hippocampus, and a reduction in brain volume.

Long-term alcohol use and abuse may affect several aspects of cognitive ability including attention, learning and memory. It has also been suggested that 29 per cent of dementia is alcohol-related. Alcohol-related dementia is linked to cognitive decline, mental confusion and severe memory impairments.

‘Legal highs’

Novel psychoactive substances are drugs that produce effects similar to cocaine and cannabis, but are not covered by the UK Misuse of Drugs Act. One of the most popular legal highs is nitrous oxide – the gas used as mild anaesthetic in dental surgery. It is the second-most popular recreational drug in the UK, after cannabis, probably because it is cheap and easy to obtain. In six years, nitrous oxide has caused 17 deaths and has led to calls for a change in the law.

When inhaled, nitrous oxide gas dissolves into the bloodstream and reaches the brain within seconds. While its action on the brain is not well understood, it is believed to prevent glutamate from binding to NMDA (N-methyl-D-aspartate) receptors.

An increase in nitrous oxide decreases the amount of oxygen available to the brain. Most nitrous-oxide-related deaths are caused by brain injury following unconsciousness or hypoxia (lack of oxygen). This mix of increased nitrous oxide and reduced oxygen has been associated with an increase in brain-cell death, especially in areas of the brain associated with learning and memory. Longer-term, it can affect how your body uses vitamin B12, which is essential for maintaining the myelination of neurons (the protective layer that surrounds nerve cells). Using nitrous oxide has also been associated with an increased risk of heart attacks.

Nitrous oxide doesn’t seem to be very physically addictive, but the shortness of the high means people often go back for more – and it is relatively easy to obtain. This can lead to psychological addiction, which puts the user at increased risk of brain damage from repeated use.

Lead image:

SBC9/Flickr CC BY NC

References

Further reading

About this resource

This resource was first published in ‘Addiction’ in September 2015.

Topics:
Ecology and environment, Psychology, Health, infection and disease
Issue:
Addiction
Education levels:
16–19, Continuing professional development