Smoking and its impact on eating behavior: A review

May combine two claims.

Smokers exhibit reduced sensitivity to sweet and bitter tastes, which may influence their consumption of highly palatable, energy-dense foods.

“Literature suggests that smokers exhibit reduced sensitivity to sweet and bitter tastes, which may influence their consumption of highly palatable, energy-dense foods [7].”

• cites [7] Pepino MY Mennella JA Alcohol Clin Exp Res. 2007 31 1891 17949394 PMC2268904 sourcePartly supported

  The Discussion reports reduced sweet-taste sensitivity in the women studied and cites studies suggesting reduced bitter-taste sensitivity in smokers. The Conclusions say smoking may alter sweet preferences, but describe the sweet-taste literature as equivocal and the reasons for the association with sweet consumption as unknown. The proposed effect of taste sensitivity on consumption of energy-dense foods is therefore plausible in this paper, not established. (LLM, conf=0.82)

  Experimental — accuracy not yet measured

May combine two claims.

Smoking significantly influences eating behavior through physiological mechanisms primarily mediated by nicotine, including appetite suppression, altered metabolism and energy balance, and effects on hunger-related hormones such as ghrelin and leptin.

“Smoking significantly influences eating behavior through various physiological mechanisms, primarily mediated by nicotine. These mechanisms include appetite suppression, alteration in metabolism and energy balance and impact on hunger-related hormones such as ghrelin and lepton [2, 9].”

• cites [2] Alruwaili A Appetite. 2025 214 108194 40513832 sourceNot checked — no full text of the source
• cites [9] Jo YH J Neurobiol. 2002 53 618 12436425 PMC2367209 sourcePartly supported

  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 measured

• AssumptionRests on an assumption: Nicotine is the primary psychoactive and addictive component of tobacco.

May combine two claims.

Nicotine interacts with the brain's reward system and alters neurotransmitter activity, particularly dopamine and serotonin, which play key roles in hunger and satiety regulation.

“Studies have shown that nicotine interacts with the brain's reward system and alters neurotransmitter activity, particularly dopamine and serotonin, which play key roles in hunger and satiety regulation [2, 3, 4, 5-6].”

• cites [2] Alruwaili A Appetite. 2025 214 108194 40513832 sourceNot checked — no full text of the source
• cites [3] Alruwaili A Addiction. 2024 119 1737 38884138 sourceNot checked — no full text of the source
• cites [4] Blanco-Gandia MC World J Psychiatry. 2021 11 517 34631457 PMC8475000 sourcePartly supported

  The Introduction (page unavailable) says that drugs and food engage reward pathways through dopamine release, which can alter the control of hunger and satiety. The common-neurobiology section also identifies dopamine as a regulator of feeding behavior and drug addiction. Neither passage establishes the claim specifically for nicotine or identifies serotonin as involved; a search for serotonin found no supporting passage. (LLM, conf=0.85)

  Experimental — accuracy not yet measured
• cites [5] Audrain-Mcgovern J Benowitz NL. Clin Pharmacol Ther. 2011 90 164 21633341 PMC3195407 sourceSupported
• cites [6] Mineur YS Science. 2011 332 1330 21659607 PMC3113664 sourcePartly supported

  The paper reports that nicotine activates hypothalamic POMC neurons through nicotinic acetylcholine receptors and decreases food intake in mice (Abstract; no page given). It does not establish the claimed reward-system mechanism or identify dopamine and serotonin as the neurotransmitters involved in hunger and satiety regulation; searches for those terms found no supporting passage. (LLM, conf=0.84)

  Experimental — accuracy not yet measured

May combine two claims.

Nicotine has appetite-suppressing effects, leading many smokers to report reduced food intake.

“Nicotine, the primary psychoactive component of tobacco, is known to cause appetite-suppressing effects leading many smokers to report reduced food intake on one hand”

• Also stated in: § Background: · boosted

  “Nicotine, the primary psychoactive component of tobacco, is known to have appetite- suppressing effects, leading many smokers to report reduced food intake and weight control as a motivation for smoking.”

• cites [2] Alruwaili A Appetite. 2025 214 108194 40513832 sourceNot checked — no full text of the source
• cites [3] Alruwaili A Addiction. 2024 119 1737 38884138 sourceNot checked — no full text of the source
• cites [4] Blanco-Gandia MC World J Psychiatry. 2021 11 517 34631457 PMC8475000 sourceCould not verify

  The paper’s References section mentions a study of nicotine, food deprivation, and resistance to smoking, but that title does not address whether nicotine suppresses appetite. Searches for nicotine, appetite suppression, and smokers’ food intake found no passage in our copy reporting that smokers eat less because of nicotine. (LLM, conf=0.76)

  Experimental — accuracy not yet measured
• cites [5] Audrain-Mcgovern J Benowitz NL. Clin Pharmacol Ther. 2011 90 164 21633341 PMC3195407 sourcePartly supported

  The Physiology of Smoking Effect on Body Weight section describes nicotine’s appetite-suppressing effects, and the Natural History section says food intake can increase after smoking cessation. Neither section says that many smokers report reduced food intake; that self-report claim is not supported by our copy. Page numbers are unavailable. (LLM, conf=0.85)

  Experimental — accuracy not yet measured
• cites [6] Mineur YS Science. 2011 332 1330 21659607 PMC3113664 sourcePartly supported

  The Abstract says smoking decreases appetite, and the paper reports that nicotine decreases food intake in mice. It also says smokers often report smoking to control their weight, but it does not say that many smokers report reduced food intake. (LLM, conf=0.83)

  Experimental — accuracy not yet measured

• AssumptionRests on an assumption: Nicotine is the primary psychoactive and addictive component of tobacco.

May combine two claims.

Nicotine stimulates the hypothalamic melanocortin system, and its interaction with melanocortin-4 receptors contributes to appetite suppression, decreasing appetite and increasing metabolism.

“Nicotine also stimulates the hypothalamic melanocortin system, which plays a crucial role in regulating feeding behavior and energy homeostasis. This activation leads to reduced food intake and consequently, weight loss [5]. Further, studies suggest that nicotine's interaction with the central melanocortin system, particularly the melanocortin-4 receptors, also contributes to appetite suppression.”

• cites [8] Filozof C Obes Rev. 2004 5 95 15086863 sourceNot checked — no full text of the source
• cites [9] Jo YH J Neurobiol. 2002 53 618 12436425 PMC2367209 sourcePartly supported

  The Introduction reports that nicotine suppresses food intake and discusses the lateral hypothalamus as a possible site of action. It separately explains that MC4 receptor signaling normally limits food intake and body fat, but does not show that nicotine stimulates the melanocortin system or acts through MC4 receptors. It also says findings on nicotine-induced changes in overall metabolic rate are variable, rather than establishing increased metabolism. (LLM, conf=0.88)

  Experimental — accuracy not yet measured

• AssumptionRests on an assumption: Nicotine is the primary psychoactive and addictive component of tobacco.

May combine two claims.

Marketing and advertisements of food substances through media and socioeconomic status including income, education and occupation influence consumer's choice of dietary patterns.

“Marketing and advertisements of such food substances through media and the socioeconomic status of the individual including income, education and occupation also influence consumer's choice of dietary patterns [28, 29].”

• cites [28] Smith R Nutrients. 2019 11 875Not matched

  Couldn’t be matched to a paper in Crossref, so it can’t be checked.

• cites [29] Darmon N Drewnowski A Nutr Rev. 2015 73 643 26307238 PMC4586446 sourcePartly supported

  The Results and Discussion section (page unavailable) links socioeconomic status with diet quality and describes differences associated with income, parental education, and occupation. The cited paper does not establish the sentence’s separate claim that marketing and media advertisements influence dietary choices. (LLM, conf=0.85)

  Experimental — accuracy not yet measured

May combine two claims.

Smoking raises leptin levels, while cessation lowers them, though reverse is also true in few other studies.

“It has been shown in previous studies that smoking raises leptin levels, while cessation of smoking lower the levels, whereas, the reverse is also true in few other studies [13].”

• cites [13] Shaheen N Front Psychiatry. 2023 14 1296764 38111614 PMC10725976 sourceSupported

May combine two claims.

Nicotine is a potent appetite suppressant that activates specific brain pathways to reduce hunger sensations.

“Nicotine, the primary addictive component in tobacco, has been identified as a potent appetite suppressant. Literature indicates that nicotine activates specific pathways in the brain that reduce hunger sensations.”

• cites [5] Audrain-Mcgovern J Benowitz NL. Clin Pharmacol Ther. 2011 90 164 21633341 PMC3195407 sourcePartly supported

  The Physiology of Smoking Effect on Body Weight section says nicotine acts on brain receptors and that its acute effects activate systems that decrease appetite. But it also says chronic changes are consistent with increased appetite; the unqualified description of nicotine as a potent appetite suppressant overstates the paper. The section discusses appetite and eating, rather than directly measuring hunger sensations; page numbers were not available in our copy. (LLM, conf=0.85)

  Experimental — accuracy not yet measured

• AssumptionRests on an assumption: Nicotine is the primary psychoactive and addictive component of tobacco.

May combine two claims.

Smoking is associated with an unhealthy distribution of body fat, particularly increased visceral fat, which elevates risk of heart disease, stroke and metabolic disorders such as insulin resistance and type 2 diabetes.

“However, smoking is also associated with an unhealthy distribution of body fat, particularly an increase in visceral fat, which elevates the risk of heart disease, stroke and metabolic disorders such as insulin resistance and type 2 diabetes [5].”

• cites [5] Audrain-Mcgovern J Benowitz NL. Clin Pharmacol Ther. 2011 90 164 21633341 PMC3195407 sourcePartly supported

  The Physiology section (page unavailable) says smokers have a higher proportion of visceral fat and that a high waist-to-hip ratio is a cardiovascular risk factor. The Treatment section (page unavailable) also links smokers’ high visceral-to-subcutaneous fat ratio to cardiovascular risk. The paper associates increased visceral fat with insulin resistance and says smoking can cause diabetes, but it does not say that visceral fat itself elevates the risk of stroke, insulin resistance, or type 2 diabetes. (LLM, conf=0.86)

  Experimental — accuracy not yet measured

May combine two claims.

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.”

• cites [14] Benowitz NL N Engl J Med. 2010 362 2295 20554984 PMC2928221 sourcePartly supported

  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 measured
• cites [15] Volkow ND Trends Cogn Sci. 2010 15 37 21109477 PMC3124340 sourcePartly supported

  In “Food is a potent natural reward and conditioning stimulus” (page not available), the paper says eating palatable food releases dopamine and links dopamine to food reward and motivation to eat. It does not establish the smoking-specific part of the claim; searches for smoking and nicotine found no passage addressing it. (LLM, conf=0.85)

  Experimental — accuracy not yet measured

May combine two claims.

Nicotine 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.”

• cites [14] Benowitz NL N Engl J Med. 2010 362 2295 20554984 PMC2928221 sourcePartly supported

  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

• AssumptionRests on an assumption: Nicotine is the primary psychoactive and addictive component of tobacco.

May combine two claims.

Smokers may use smoking instead of eating to cope with stress, leading to decreased food intake and body weight; after smoking cessation, these individuals may be more susceptible to weight gain when eating is used to cope with stress.

“Literature has shown that smokers may use smoking instead of eating to cope with stress, leading to decreased food intake and body weight. However, after smoking cessation, these individuals may be more susceptible to weight gain when eating is used to cope with stress (Stress eating) [21].”

• cites [21] Lengsfeld S Trials. 2023 24 284 37081574 PMC10120253 sourcePartly supported

  The Introduction (Background and rationale; page not provided) reports that people who quit smoking gain an average of 4–5 kg within 12 months. It does not say that smokers use cigarettes instead of food to cope with stress, that this decreases food intake or weight, or that stress eating explains weight gain after cessation. (LLM, conf=0.87)

  Experimental — accuracy not yet measured

May combine two claims.

Foods high in sugar, fat and salt increase dopamine levels in the nucleus accumbens and reinforce eating habits, especially during stress or boredom.

“Similarly, foods high in sugar, fat and salt also increase dopamine levels in the nucleus accumbens. Similar to nicotine, highly palatable foods stimulate reward centers and reinforce the habit of eating, especially during stress or boredom.”

• cites [15] Volkow ND Trends Cogn Sci. 2010 15 37 21109477 PMC3124340 sourcePartly supported

  The section “Food is a potent natural reward and conditioning stimulus” says that foods rich in sugar and fat are potent rewards that promote eating and conditioning. It also describes increased dopamine release in the nucleus accumbens on initial exposure to a food reward. Our copy does not extend those findings to salt or say that stress or boredom especially reinforces eating habits. (LLM, conf=0.87)

  Experimental — accuracy not yet measured

May combine two claims.

Smoking is associated with decreased sensitivity to sweet, which may influence food preferences and consumption patterns.

“Additionally, smoking has been associated with decreased sensitivity to sweet. Literature indicates that smokers have a reduced ability to perceive sweetness, which may influence their food preferences and consumption patterns [7].”

• cites [7] Pepino MY Mennella JA Alcohol Clin Exp Res. 2007 31 1891 17949394 PMC2268904 sourceSupported

May combine two claims.

Smoking impairs gustatory sensitivity, leading to diminished taste perception; smokers exhibit significantly decreased taste sensation compared to non-smokers, with higher nicotine dependence correlating with greater taste deficits.

“Cigarette smoking can impair gustatory sensitivity, leading to diminished taste perception. Studies have found that smokers exhibit significantly decreased taste sensation compared to non- smokers, with higher nicotine dependence correlating with greater taste deficits.”

• cites [17] Chéruel F Tob Induc Dis. 2017 15 15 28261024 PMC5329949 sourceSupported

May combine two claims.

Repeated 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].”

• cites [14] Benowitz NL N Engl J Med. 2010 362 2295 20554984 PMC2928221 sourcePartly supported

  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 measured

May combine two claims.

Peer influence has strong associations with both smoking initiation and continuation and food intake across various age groups, especially among adolescents and young adults.

“Peer influence significantly has strong associations with both smoking initiation and continuation and food intake across various age groups, especially among adolescents and young adults.”

• cites [25] Liu J Psychol Bull. 2017 143 1082 28771020 PMC5789806 sourcePartly supported

  The Discussion (page unavailable) reports significant associations between peer smoking and both smoking initiation and continuation among adolescents. The Results describe samples with a mean age of approximately 14–15 years. The cited paper does not establish the claim about food intake or extend its findings across various age groups, including young adults. (LLM, conf=0.90)

  Experimental — accuracy not yet measured
• cites [26] Stok FM Health Psychol Rev. 2016 10 326 26878931 sourcePartly supported

  The Results report significant associations between peer social norms and young people's food intake in 16 of 17 correlational studies; the Discussion reports evidence of a relation in 32 of 33 studies overall. The review covers ages 10–25 and reports similar food-intake findings across that range, but the passages do not support the claim about smoking initiation or continuation, or extend the food-intake finding to older age groups. (LLM, conf=0.88)

  Experimental — accuracy not yet measured

May combine two claims.

Smokers often have higher total caloric intake and consume more carbohydrates than non-smokers, though differences may be influenced by lifestyle and demographic variables.

“In terms of macronutrient consumption, studies have shown that smokers often have higher total caloric intake and consume more carbohydrates than non-smokers. However, these differences in macronutrient intake may be influenced by various factors, including lifestyle and demographic variables [20].”

• cites [20] Jitnarin N Asia Pac J Public Health. 2014 26 481 22186385 PMC4824046 sourcePartly supported

  The Results report higher total caloric and carbohydrate intake among male smokers than male nonsmokers, but no significant difference in those intakes among women. The Statistical Analyses section stratifies dietary comparisons by gender; it does not establish that lifestyle or other demographic variables explain the intake differences. Page numbers are unavailable in our copy. (LLM, conf=0.87)

  Experimental — accuracy not yet measured

May combine two claims.

Smoking is associated with varied dietary patterns and a complex relationship with eating behaviors.

“Smoking and its association with eating and dietary behaviors is complex, with smokers exhibiting varied dietary patterns.”

Probably not a substantial claim: may not pass S4 (based).

Nicotine can cause increased appetite leading to obesity.

“and causing increased appetite leading to obesity on the other.”

• AssumptionRests on an assumption: Nicotine is the primary psychoactive and addictive component of tobacco.

May combine two claims.

Individuals who quit smoking typically gain between 3 to 9 kilograms within the first eight years of cessation, with most weight gain occurring within the initial six months.

“Studies have shown that individuals who quit smoking typically gain between 3 to 9 kilograms within the first eight years of cessation, with most weight gain occurring within the initial six months.”

• cites [3] Alruwaili A Addiction. 2024 119 1737 38884138 sourceNot checked — no full text of the source

May combine two claims.

Nicotine increases energy expenditure by raising resting metabolic rate and promoting lipolysis, leading to increased fat metabolism and reduced body weight.

“Nicotine increases energy expenditure by raising the resting metabolic rate and promoting lipolysis, the breakdown of fats. This leads to increased fat metabolism and a reduction in body weight [10].”

• cites [10] Chiolero A Am J Clin Nutr. 2008 87 801 18400700 sourceNot checked — no full text of the source

• AssumptionRests on an assumption: Nicotine is the primary psychoactive and addictive component of tobacco.

May combine two claims.

Diminished sensitivity to sweetness and other tastes may drive smokers to seek more intensely flavored or higher-calorie foods, leading to a preference for energy-dense foods and unhealthy dietary patterns.

“The diminished sensitivity to sweetness and other taste might drive smokers to seek more intensely flavored or higher-calorie foods to achieve the desired sensory experience. This compensatory behavior can result in a preference for energy- dense foods, contributing to unhealthy dietary patterns [18].”

• cites [18] Chao AM Eat Behav. 2016 24 61Not matched

  Couldn’t be matched to a paper in Crossref, so it can’t be checked.

May combine two claims.

Ghrelin levels in blood might increase while smoking cigarettes and decline upon quitting.

“According to some studies in the literature, ghrelin levels in the blood might increase while smoking cigarettes and decline upon quitting the habit [2, 12].”

• cites [2] Alruwaili A Appetite. 2025 214 108194 40513832 sourceNot checked — no full text of the source
• cites [12] Kojima M Nature. 1999 402 656Not matched

  Couldn’t be matched to a paper in Crossref, so it can’t be checked.

May combine two claims.

Cessation of nicotine intake removes its appetite-suppressing effects, often leading to increased hunger and a preference for high-calorie foods.

“Moreover, cessation of nicotine intake removes its appetite-suppressing effects, often leading to increased hunger and a preference for high-calorie foods.”

May combine two claims.

Nicotine exerts significant appetite-suppressing effects through central pathways, and its cessation often leads to increased hunger and hedonic eating behaviors.

“Nicotine exerts significant appetite suppressing effects through central pathways on one hand and its cessation often leads to increased hunger and hedonic eating behaviors, on the other.”

May combine two claims.

Post-cessation weight gain can diminish some health benefits of quitting, such as improvements in lung function, and may increase risk of type 2 diabetes and hypertension.

“This post-cessation weight gain can diminish some health benefits of quitting, such as improvements in lung function and may increase the risk of developing type 2 diabetes and hypertension [3].”

• cites [3] Alruwaili A Addiction. 2024 119 1737 38884138 sourceNot checked — no full text of the source