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Biological Aspects of the Link between Smoking and Depression
Abstract
A link between smoking and depressive symptoms has been described in the literature for over a decade. The neurotransmitter systems affected by cigarette smoke mirror the neurotransmitter pathways thought to be involved in the biological mechanisms of depression. Cigarette smoke contains several psychoactive chemicals; nicotine is the best studied among these and is widely accepted to be the addictive substance in tobacco. Nicotine binds to nicotinic receptors in the brain, augmenting the release of numerous neurotransmitters, including dopamine, serotonin, norepinephrine, acetylcholine, gamma-aminobutyric acid, and glutamate. Cigarette smoke has other psychoactive properties apart from nicotinic receptor stimulation. For example, it inhibits monoamine oxidase (the enzyme responsible for breaking down the biogenic amine neurotransmitters norepinephrine, serotonin, and dopamine) in the brain. Various antidepressants act through modulation of the biogenic amine neurotransmitter pathways. That the neural substrates modified by both smoking and antidepressant drugs overlap has relevance to smoking cessation. The use of antidepressants as adjuvants to smoking-cessation treatment can enhance cessation success rates. Understanding the neurobiological mechanisms underlying the association between smoking and depression may improve physicians' ability to assist smokers in their efforts to quit and will contribute to a more thorough comprehension of both the biology of addiction and th…
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“Population-based studies show that smokers are twice as likely as nonsmokers to have a lifetime history of major depression (11–13).”
From Persistent β 2 *-Nicotinic Acetylcholinergic Receptor Dysfunction in Major Depressive Disorder (2012) · cites this paper as [12]
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Metadata
- Authors
- Quattrocki, E., Baird, A., & Yurgelun-Todd, D.
- Affiliations
- Harvard University (US)
- Venue
- Harvard Review of Psychiatry
- Published
- 2000-09
- Volume
- 8
- Issue
- 3
- Pages
- 99-110
- ISSN
- 1067-3229 (ISSN-L)
- OpenAlex
- W2022451998
- Cited by
- 176
- References
- 101
- Citations by year
- 2026: 4 · 2025: 5 · 2024: 6 · 2023: 3 · 2022: 6 · 2021: 6 · 2020: 1 · 2018: 6 · 2017: 1 · 2016: 7 · 2015: 6 · 2014: 10 · 2013: 11 · 2012: 3
- FWCI
- 4.28
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Harvard Review of Psychiatry (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Health Sciences › Medicine › Public Health, Environmental and Occupational Health › Smoking Behavior and Cessation
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Nicotinic Acetylcholine Receptors Study
- Health Sciences › Medicine › Pharmacology (medical) › Treatment of Major Depression
- Keywords
- smoking, depression, nicotine, nicotinic acetylcholine receptors, neurotransmitters, monoamine oxidase inhibition, antidepressants, smoking cessation, nicotine dependence, dopamine, serotonin, norepinephrine
- MeSH terms
- Smoking Prevention, Affect, Brain, Cognition, Depression, Humans, Monoamine Oxidase, Nicotine, Receptors, Nicotinic, Reinforcement, Psychology, Smoking, Smoking Cessation, Neurotransmitter Agents
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
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