Nicotine addiction
Open accessAbstract
This review gives an account of the cigarette as a highly efficient nicotine delivery system. It explains how nicotine induces pleasure, reduces stress and anxiety, and causes addiction to tobacco smoking. The basis of nicotine addiction rests on its effects on the brain, but addiction is also influenced by learned or conditioned factors, genetics, and social and environmental conditions.
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With repeated exposure to nicotine, tolerance develops and induces signs of physical dependence and withdrawal symptoms.
“With repeated exposure to nicotine, tolerance develops and induces signs of physical dependence and withdrawal symptoms”
From Prenatal nicotine exposure during pregnancy results in adverse neurodevelopmental alterations and neurobehavioral deficits (2023) · cites this paper as [18]
The Neuroadaptation section says repeated nicotine exposure produces tolerance and links receptor desensitization to dependence. It says craving and withdrawal begin during abstinence, when desensitized receptors become responsive; it does not say tolerance itself induces withdrawal symptoms. (LLM, conf=0.82)
Experimental — accuracy not yet measurednAChRs are pentameric cation-selective ligand-gated ion channels composed of α and β subunits that can signal release of neurotransmitters such as dopamine, norepinephrine, acetylcholine, GABA, and glutamate involved in reward pathways, neuromuscular junction transmission, and cognition.
“nAChRs are pentameric cation-selective ligand-gated ion channels composed of α and β subunits ( α 1–7, 9–10; β 1–4) that can signal the release of neurotransmitters such as dopamine, norepinephrine, acetylcholine, GABA, and glutamate involved in reward pathways, transmission at the neuromuscular junction, and cognition (Figures 2, 3)”
From Prenatal nicotine exposure during pregnancy results in adverse neurodevelopmental alterations and neurobehavioral deficits (2023) · cites this paper as [18]
Split into 2 atoms — 1 confirmed, 1 partially supported, 0 disputed, 0 misattributed, 0 unverifiable. Expand the claim to see per-atom verdicts.
Experimental — accuracy not yet measuredWhen individuals quit smoking, absence of nicotine-induced dopamine release can lead to compensatory behaviors, most commonly increased food intake.
“When individuals quit smoking, the absence of nicotine- induced dopamine release can lead to compensatory behaviors, most commonly increased food intake.”
From Smoking and its impact on eating behavior: A review (2026) · cites this paper as [14]
The “Nicotine and Neurotransmitter Release” section says nicotine releases dopamine and links dopamine to the drive to eat. “Neuroadaptation” links reduced dopaminergic activity to nicotine withdrawal. The paper does not say that quitting prompts compensatory eating or that increased food intake is the most common such behavior. (LLM, conf=0.85)
Experimental — accuracy not yet measuredRepeated nicotine exposure sensitizes the reward system and strengthens associations between environmental cues and dopamine release.
“Repeated nicotine exposure sensitizes the reward system and strengthens associations between environmental cues (like the sight or smell of cigarettes) and dopamine release [14].”
From Smoking and its impact on eating behavior: A review (2026) · cites this paper as [14]
The ‘Nicotine and Neurotransmitter Release’ section says nicotine increases responsiveness to reward and releases dopamine. ‘Conditioned Behavior’ says regular smoking links environmental cues to nicotine’s rewarding effects, but it does not say those cues become associated specifically with dopamine release. (LLM, conf=0.84)
Experimental — accuracy not yet measuredNicotine activates nicotinic acetylcholine receptors on dopaminergic neurons in the VTA, increasing dopamine release in the nucleus accumbens, resulting in pleasurable sensations, stress relief and mood enhancement.
“Nicotine, the addictive substance in tobacco, activates nicotinic acetylcholine receptors (NACHRS) on dopaminergic neurons in the ventral tegmental area (VTA). This activation increases dopamine release in the nucleus accumbens (NAC), a central part of the brain's reward system, resulting in pleasurable sensations, stress relief and mood enhancement.”
From Smoking and its impact on eating behavior: A review (2026) · cites this paper as [14]
The Brain Mechanisms sections say nicotine binds nicotinic receptors, releases dopamine, and engages reward-related neurons in the VTA and nucleus accumbens. The Psychoactive Effects section says nicotine reduces stress and helps regulate mood, but the copy does not establish that dopamine release in the nucleus accumbens causes those particular effects. (LLM, conf=0.85)
Experimental — accuracy not yet measured
Both smoking and eating highly palatable foods stimulate the dopamine system, reinforcing these behaviors.
“Both smoking and eating, particularly highly palatable foods stimulate the dopamine system, reinforcing these behaviors.”
From Smoking and its impact on eating behavior: A review (2026) · cites this paper as [14]
The Brain Mechanisms section says nicotine releases dopamine and that dopamine is important to nicotine’s reinforcing effects and to drives such as eating. It does not specifically discuss highly palatable foods, so that qualification is not supported by our copy. (LLM, conf=0.86)
Experimental — accuracy not yet measuredStimulation of nAChRs in dopaminergic neurons of the VTA and in the shell of the NA is critical in drug-induced reward pathways important for perception of pleasure and reward.
“Importantly, stimulation of nAChRs in dopaminergic neurons of the VTA of the midbrain and in the shell of the NA are critical in drug-induced reward pathways that are important for the perception of pleasure and reward”
From Prenatal nicotine exposure during pregnancy results in adverse neurodevelopmental alterations and neurobehavioral deficits (2023) · cites this paper as [18]
In a given year, only 3% of smokers successfully quit, while 70% express a desire to quit.
“However, in a given year, only 3% of smokers are actually successful in their cessation attempts, even though 70% of smokers express desire to quit [6].”
From Mechanistic insights into nicotine withdrawal (2011) · cites this paper as [6]
Supplementing nicotine during abstinence eases transition from smoking to complete abstinence by relieving withdrawal and nicotine craving.
“supplementing the user with nicotine during abstinence will ease the transition from smoking to complete abstinence by relieving withdrawal and nicotine craving [6, 208].”
From Mechanistic insights into nicotine withdrawal (2011) · cites this paper as [6]
Nicotine exerts its rewarding effects by acting at nAChRs and increasing neurotransmission in the mesolimbic and nigrostriatal dopaminergic pathways.
“Nicotine seems to exert its rewarding effects by acting at nicotinic acetylcholine receptors (nAChRs) and increasing neurotransmission in the mesolimbic and nigrostriatal dopa-minergic pathways”
From Varenicline Is a Potent Partial Agonist at α6β2* Nicotinic Acetylcholine Receptors in Rat and Monkey Striatum (2012) · cites this paper as Benowitz, 2010
Smoking can be seen as a psychobiological stressor as it can damage the nervous system and there is evidence that neurological systems and oxidative stress pathways and inflammation markers return to normal functioning after sustained smoking cessation.
“Smoking can be seen as a psychobiological stressor as it can damage the nervous system (Benowitz, 2010; Hallstrand et al., 2014; Salem et al., 2021) and there is evidence that neurological systems and oxidative stress pathways and inflammation markers return to normal functioning after sustained smoking cessation (Mamede et al., 2007; Salem et al., 2021).”
From An application of the stress-diathesis model: A review about the association between smoking tobacco, smoking cessation, and mental health (2023) · cites this paper as Benowitz, 2010
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- Authors
- Benowitz, N. L.
- Affiliations
- San Francisco General Hospital (US)
- Corresponding author
- Benowitz, Neal L.
- ORCID
- Benowitz, Neal L.
- Venue
- New England Journal of Medicine
- Publisher
- Massachusetts Medical Society
- Published
- 2010-06-17
- Volume
- 362
- Issue
- 24
- Pages
- 2295-2303
- ISSN
- 0028-4793 (ISSN-L)
- 1533-4406
- PMC
- PMC2928221
- OpenAlex
- W4231752535
- Cited by
- 1,508
- References
- 76
- Citations by year
- 2026: 93 · 2025: 117 · 2024: 109 · 2023: 115 · 2022: 124 · 2021: 145 · 2020: 139 · 2019: 104 · 2018: 96 · 2017: 76 · 2016: 70 · 2015: 67 · 2014: 83 · 2013: 57 · 2012: 57
- FWCI
- 5.35
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- New England Journal of Medicine (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- Funders
- U.S. Public Health Service
- National Institute on Drug Abuse (DA20830, DA02277, R01DA002277, U01DA020830, R37DA002277)
- Topics
- Health Sciences › Medicine › Physiology › Smoking Behavior and Cessation
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Nicotinic Acetylcholine Receptors Study
- Health Sciences › Medicine › Epidemiology › Substance Abuse Treatment and Outcomes
- Keywords
- nicotine dependence, cigarette smoking, nicotine delivery, pleasure, stress reduction, anxiety, conditioned learning, addiction genetics, socio-environmental factors
- MeSH terms
- Female, Humans, Limbic System, Male, Nicotine, Receptors, Nicotinic, Risk Factors, Smoking, Substance Withdrawal Syndrome, Tobacco Use Disorder
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