How Nicotine and Alcohol Each Change the Brain to Increase Craving for the Other | Research

The takeaway

A review described how chronic nicotine and alcohol each alter multiple brain systems including cannabinoid receptors, creating cross-drug changes that lower withdrawal symptoms from each other and increase preference for combined use.

Read this if you use both tobacco and alcohol and want to understand why they go together.

Nicotine and alcohol each altered cannabinoid receptors and reduced each other's withdrawal

What the researchers found

This review examined the neurochemical interactions between nicotine and alcohol, two substances whose use frequently co-occurs.

Chronic nicotine altered multiple brain systems: nicotinic receptors (subunit composition changes), catecholamine, glutamate, GABA levels, and opiate and cannabinoid receptors. Similarly, chronic alcohol affected many of the same systems.

Key interactions included:

- The two substances reduced each other's negative withdrawal symptoms, which may reinforce combined use

- Some brain changes from combined use were additive, while others were opposing

- Effects were sex- and age-dependent, with adolescents generally more sensitive

- Endocannabinoid content was among the systems affected by both substances

The authors noted that the mechanisms by which one drug increases preference for another are complex, multi-component, and likely differ depending on the direction of the interaction.

Why it matters

Smoking and drinking co-occur at very high rates. Understanding the neurochemical basis for this co-use could lead to treatments that address both substances simultaneously rather than treating them separately.

The numbers in context

Brain systems affected: nicotinic receptors, catecholamines, glutamate, GABA, opioid peptides, cannabinoid receptors, endocannabinoid content. Effects were sex- and age-dependent.

How the study worked

Narrative review examining neurochemical changes induced by chronic nicotine and alcohol, focusing on mechanisms of cross-drug preference enhancement.

What this study cannot tell us

Narrative review without systematic methodology. Many findings were from animal studies that may not translate to human experience. The complexity of multi-system interactions makes specific conclusions difficult.

How to read the evidence

Comprehensive narrative review of primarily preclinical evidence on complex multi-system drug interactions.

When this study was published

Published in 2010. Research on nicotine-alcohol interactions has continued, with increasing attention to the endocannabinoid system as a mediator.

The bigger picture

The interaction between nicotine, alcohol, and the cannabinoid system highlights how substance use is not isolated to single neurotransmitter systems. Each drug changes the landscape for other drugs, creating complex patterns of co-use and cross-dependence.

Questions still open

Could targeting the endocannabinoid system help treat co-occurring nicotine and alcohol use? Do the opposing effects of combined use create unpredictable outcomes? Should treatment programs address all co-used substances simultaneously?

Common questions

Why do smoking and drinking go together?

At the brain level, each substance changes neural systems in ways that reduce withdrawal from the other and increase preference. They essentially make each other more rewarding and less aversive, creating a powerful reinforcement loop.

Does the endocannabinoid system play a role?

Yes, both nicotine and alcohol affect endocannabinoid content and cannabinoid receptors. The endocannabinoid system appears to be one of several neural systems that mediate the cross-drug preference enhancement.

Read the original research

Nicotine: alcohol reward interactions.

Neurochemical research, 35(8), 1248-58

View on PubMed ↗Publisher’s paper ↗

Citation

Lajtha, A; Sershen, H. (2010). Nicotine: alcohol reward interactions.. Neurochemical research, 35(8), 1248-58. https://doi.org/10.1007/s11064-010-0181-8