Nicotine and Type 1 Diabetes: The Research

Table of Contents

1. Research at a Glance
2. The Papers
3. PubMed Topic Searches
4. More Nicotine Research
5. Connections
6. Featured Videos

Research at a Glance

What kind of study each paper on this page is, and when the papers were published. Hover over a bar for its count.

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The Papers (16)

Newest first. Study types on this page — Human trial: 3 · Human observational study: 4 · Review: 3 · Animal study: 5 · Cell study: 1. Each summary is written from the paper’s own abstract; follow the PubMed link for the full record.

Joint effect of nicotine use and diabetes distress on glycemic control in young adults with type 1 diabetes

Human observational study, 2025. This study looked at 388 young adults with type 1 diabetes whose blood sugar was above the target range, using a national cross-sectional analysis of data from a clinical trial. Vaping was the most common way they used nicotine. People who used a lot of nicotine and also had more diabetes-related distress had worse blood sugar control on objective measures. The authors note that nicotine inhibits glucose metabolism.

Plaitano EG, Stanger C (2025). Joint effect of nicotine use and diabetes distress on glycemic control in young adults with type 1 diabetes. J Diabetes Complications. — PubMed PMID: 40398346 · doi:10.1016/j.jdiacomp.2025.109083

Smoking and diabetes

Review, 2024. This review discusses how smoking raises insulin resistance and impairs insulin-producing beta cells through several mechanisms, though exactly how is not fully understood. It notes that mechanistic studies have mostly tested nicotine as the agent responsible, but says that because other tobacco ingredients were rarely studied separately, it cannot be concluded that nicotine alone explains the increased diabetes risk. Smoking also worsens blood sugar control and increases complications and death risk in both type-1 and type-2 diabetes. The paper is a review discussing treatment approaches, including smoking-cessation drugs, for people with diabetes who smoke.

Rouland A, Thuillier P, Al-Salameh A et al. (2024). Smoking and diabetes. Ann Endocrinol (Paris). — PubMed PMID: 39218351 · doi:10.1016/j.ando.2024.08.001

Attenuated Tregs increase susceptibility to type 1 diabetes in prenatal nicotine exposed female offspring mice

Animal study, 2019. This study in mice looked at whether nicotine given to mothers during pregnancy raises the risk of type 1 diabetes in their female offspring. Compared with controls, the exposed offspring weighed less and had higher blood sugar from day 21 to day 42 after birth. By day 42 they also had raised levels of an autoantibody used to detect type 1 diabetes, along with smaller insulin-producing islet areas and fewer beta cells in the pancreas. They also had fewer regulatory T cells, a type of immune cell that helps prevent the immune system from attacking the body, and the authors suggest this drop may explain the diabetes-like changes. These findings come only from mice.

Zhao WH, Wen X, Qu W et al. (2019). Attenuated Tregs increase susceptibility to type 1 diabetes in prenatal nicotine exposed female offspring mice. Toxicol Lett. — PubMed PMID: 31442585 · doi:10.1016/j.toxlet.2019.08.016

Nicotine and autoimmunity: The lotus' flower in tobacco

Review, 2018. This review gathers earlier research on how nicotine affects the immune system in autoimmune diseases, including multiple sclerosis, type 1 diabetes, rheumatoid arthritis, sarcoidosis, Behçet's disease and inflammatory bowel diseases. The authors say the findings conflict. Some studies suggest nicotine increases inflammatory signals and makes a type of white blood cell (neutrophils) die and release their contents, which the immune system can then attack as if they were foreign. Other studies suggest nicotine calms inflammation, mainly by binding to the alpha-7 nicotinic receptor, which can increase regulatory T cells and lower inflammatory signals; the authors name addiction and the side effects of each nicotine product sold as the main problems with nicotine.

Gomes JP, Watad A, Shoenfeld Y (2018). Nicotine and autoimmunity: The lotus' flower in tobacco. Pharmacol Res. — PubMed PMID: 29051105 · doi:10.1016/j.phrs.2017.10.005

Activation of Nicotinic Acetylcholine Receptors Decreases Apoptosis in Human and Female Murine Pancreatic Islets

Cell study, 2016. Researchers studied isolated insulin-producing cells (islets) from mice and from humans in the lab, exposing them to inflammatory signals similar to those present early in Type 1 diabetes. They found that nicotine, as well as choline, activated nicotinic acetylcholine receptors on these cells and reduced the rate of cell death caused by the inflammatory signals. The study describes the biological steps involved, including effects on cell stress responses and calcium levels inside the cells.

Klee P, Bosco D, Guérardel A et al. (2016). Activation of Nicotinic Acetylcholine Receptors Decreases Apoptosis in Human and Female Murine Pancreatic Islets. Endocrinology. — PubMed PMID: 27471776 · doi:10.1210/en.2015-2057

Human longevity is influenced by many genetic variants: evidence from 75,000 UK Biobank participants

Human observational study, 2016. This study analyzed genetic data from over 75,000 UK Biobank participants, looking at variants linked to how long their parents lived. It found that a gene variant near a nicotinic receptor (CHRNA3), previously tied to heavier smoking and lung cancer, was associated with how long fathers survived. The study also found that people whose parents lived longer tended to carry more protective gene variants for several other conditions, including heart disease, blood pressure, and type 1 diabetes.

Pilling LC, Atkins JL, Bowman K et al. (2016). Human longevity is influenced by many genetic variants: evidence from 75,000 UK Biobank participants. Aging (Albany NY). — PubMed PMID: 27015805 · doi:10.18632/aging.100930

Short-term diabetic hyperglycemia suppresses celiac ganglia neurotransmission, thereby impairing sympathetically mediated glucagon responses

Animal study, 2015. In rats made diabetic for 7 days, the nerve cluster (celiac ganglia) that helps trigger the glucagon response to low blood sugar responded poorly to nicotine, and electrical stimulation above this cluster produced weaker norepinephrine and glucagon release, while stimulation below it was normal. A genetic mutation (WldS) that protects nerve fibers prevented this impairment, suggesting high blood sugar damages nicotine-responsive receptors in this ganglion and may explain blunted glucagon responses to low blood sugar seen early in type 1 diabetes.

Mundinger TO, Cooper E, Coleman MP et al. (2015). Short-term diabetic hyperglycemia suppresses celiac ganglia neurotransmission, thereby impairing sympathetically mediated glucagon responses. Am J Physiol Endocrinol Metab. — PubMed PMID: 26037249 · doi:10.1152/ajpendo.00140.2015

Partial blockade of nicotinic acetylcholine receptors improves the counterregulatory response to hypoglycemia in recurrently hypoglycemic rats

Animal study, 2014. Rats were given repeated episodes of low blood sugar for three days to model a condition where the body stops releasing enough hormones to fight hypoglycemia. Normally, low blood sugar triggers nicotinic acetylcholine receptors on the adrenal glands to release and produce epinephrine, but after repeated low-blood-sugar episodes this response weakened. Treating the rats with cytisine, a drug that only partially activates these same receptors (unlike nicotine, which activates them fully), improved both the epinephrine and glucagon responses during a later low-blood-sugar test.

LaGamma EF, Kirtok N, Chan O et al. (2014). Partial blockade of nicotinic acetylcholine receptors improves the counterregulatory response to hypoglycemia in recurrently hypoglycemic rats. Am J Physiol Endocrinol Metab. — PubMed PMID: 25117409 · doi:10.1152/ajpendo.00237.2014

Nicotine exposure exacerbates development of cataracts in a type 1 diabetic rat model

Animal study, 2012. Researchers gave daily nicotine injections to rats with chemically induced type 1 diabetes and compared cataract progression to diabetic rats without nicotine and to non-diabetic controls. Blood levels of inflammation markers (eotaxin, IL-6, and IL-4) rose significantly in diabetic rats, with or without nicotine, versus non-diabetic controls, and these markers trended higher still when nicotine was added to diabetes. The authors concluded that nicotine and diabetes together sped up cataract formation through inflammation-related pathways, in rats.

Tirgan N, Kulp GA, Gupta P et al. (2012). Nicotine exposure exacerbates development of cataracts in a type 1 diabetic rat model. Exp Diabetes Res. — PubMed PMID: 23049540 · doi:10.1155/2012/349320

Role of environmental chemicals in diabetes and obesity: a National Toxicology Program workshop review

Review, 2012. This is a report from a 2011 scientific workshop that reviewed existing research on whether environmental chemical exposures contribute to diabetes and obesity. Nicotine exposure during pregnancy (grouped with maternal smoking) was one of several chemical exposures considered, alongside arsenic, certain pollutants, and pesticides. The review found links between several of these exposures and type 2 diabetes, and supported the idea that early-life chemical exposure may raise obesity risk by altering fat-cell development or brain circuits that control feeding, especially when combined with a high-calorie diet later in life. The authors noted that research specifically on environmental chemicals and type 1 diabetes was very limited, calling it a critical research gap.

Thayer KA, Heindel JJ, Bucher JR et al. (2012). Role of environmental chemicals in diabetes and obesity: a National Toxicology Program workshop review. Environ Health Perspect. — PubMed PMID: 22296744 · doi:10.1289/ehp.1104597

Difficulties of smoking cessation in diabetic inpatients benefiting from a systematic consultation to help them to give up smoking

Human observational study, 2006. This study followed 306 diabetic patients admitted to a hospital's diabetes department, of whom 38 (12.4%) smoked. The smokers were younger and more often male than non-smokers, and had fewer small-blood-vessel complications but the same rate of large-blood-vessel complications. Most smokers (60%) had moderate or high nicotine dependence. All agreed to a stop-smoking consultation, but fewer than half agreed to drug treatment to help them quit, only 15% returned for a six-month follow-up visit, and only one patient had actually quit smoking by six months.

Scemama O, Hamo-Tchatchouang E, Le Faou AL et al. (2006). Difficulties of smoking cessation in diabetic inpatients benefiting from a systematic consultation to help them to give up smoking. Diabetes Metab. — PubMed PMID: 17110898 · doi:10.1016/s1262-3636(07)70301-4

Smoking is associated with an increased risk of type 2 diabetes but a decreased risk of autoimmune diabetes in adults: an 11-year follow-up of incidence of diabetes in the Nord-Trøndelag study

Human observational study, 2004. This study followed adults in Norway for 11 years to see whether smoking was linked to later diabetes. Among 738 people who became type 2 diabetics, heavy smokers (20 or more cigarettes a day) had a higher risk than non-smokers. But among people who developed autoimmune diabetes, smoking was linked to lower risk: 81 people developed latent autoimmune diabetes in adults and 18 developed classic type 1 diabetes, and smokers in these groups had a notably reduced risk compared with non-smokers. The authors concluded that nicotine affects the autoimmune processes involved in human diabetes.

Carlsson S, Midthjell K, Grill V et al. (2004). Smoking is associated with an increased risk of type 2 diabetes but a decreased risk of autoimmune diabetes in adults: an 11-year follow-up of incidence of diabetes in the Nord-Trøndelag study. Diabetologia. — PubMed PMID: 15558231 · doi:10.1007/s00125-004-1554-9

Difference between diabetic and nondiabetic smokers in the pituitary response to physical exercise

Human trial, 2004. Researchers measured hormone responses (growth hormone, cortisol, and vasopressin) to exercise on a stationary bike in 40 people: 10 smokers and 10 nonsmokers with insulin-dependent diabetes, and 10 smokers and 10 nonsmokers without diabetes. In people without diabetes, smokers had smaller increases in growth hormone and cortisol during exercise than nonsmokers, suggesting habitual nicotine intake may blunt these hormone responses. This difference between smokers and nonsmokers was not seen in the diabetic group, which the researchers suggest may be because diabetes itself alters these hormone pathways.

Coiro V, Jotti GS, Volpi R et al. (2004). Difference between diabetic and nondiabetic smokers in the pituitary response to physical exercise. Metabolism. — PubMed PMID: 15334375 · doi:10.1016/j.metabol.2004.02.019

Nicotine reduces the incidence of type I diabetes in mice

Animal study, 2002. Researchers gave nicotine to mice in two laboratory models of type 1 diabetes, an autoimmune disease in which the immune system destroys the insulin-making cells of the pancreas. In both models, mice treated with nicotine had lower blood sugar, developed diabetes less often, and kept more insulin in the pancreas. Nicotine also stopped the rise in inflammatory immune signals (IL-12, IL-1, TNF-alpha and interferon-gamma) seen in the pancreas with diabetes, and it raised calming immune signals (IL-4 and IL-10). These results come from mice only and have not been shown in people.

Mabley JG, Pacher P, Southan GJ et al. (2002). Nicotine reduces the incidence of type I diabetes in mice. J Pharmacol Exp Ther. — PubMed PMID: 11861793 · doi:10.1124/jpet.300.3.876

Effects of smoking on 24-h ambulatory blood pressure and autonomic function in normoalbuminuric insulin-dependent diabetes mellitus patients

Human trial, 1998. This study compared 24 smokers and 24 nonsmokers, all matched for sex, age and diabetes duration, who had insulin-dependent diabetes with normal urine albumin levels. Diabetic smokers had higher 24-hour average blood pressure and heart rate than diabetic nonsmokers, along with changes in heart-rate-variability measures suggesting altered nervous-system control of blood pressure. The paper notes this differs from the usual finding of lower blood pressure in smokers without diabetes, and suggests the effect may involve sustained stimulation from nicotine, possibly linked to how smoking contributes to kidney damage in diabetes.

Poulsen PL, Ebbehøj E, Hansen KW et al. (1998). Effects of smoking on 24-h ambulatory blood pressure and autonomic function in normoalbuminuric insulin-dependent diabetes mellitus patients. Am J Hypertens. — PubMed PMID: 9752895 · doi:10.1016/s0895-7061(98)00115-0

Abnormal effect of cigarette smoking on pituitary hormone secretions in insulin-dependent diabetes mellitus

Human trial, 1997. Researchers studied 10 male smokers with insulin-dependent (type 1) diabetes and 10 normal male smokers, comparing them to 10 diabetic and 10 normal non-smokers. Smoking two cigarettes raised growth hormone, vasopressin (AVP), and cortisol levels in normal subjects, and raised them even more in the diabetic smokers. During an insulin tolerance test that lowered blood sugar, smoking did not change the hormone response in normal subjects, but in diabetic subjects it significantly increased the growth hormone, vasopressin, and cortisol spikes triggered by low blood sugar. The researchers concluded that nicotine from cigarette smoking interacts with the hormone changes already seen in diabetes, boosting the body's counter-regulatory hormone response to insulin-induced low blood sugar in people with type 1 diabetes.

Chiodera P, Volpi R, Capretti L et al. (1997). Abnormal effect of cigarette smoking on pituitary hormone secretions in insulin-dependent diabetes mellitus. Clin Endocrinol (Oxf). — PubMed PMID: 9156046 · doi:10.1046/j.1365-2265.1997.1470945.x

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PubMed Topic Searches

1. PubMed: Type 1 Diabetes and nicotine (the search this page is built from)

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Connections

• Autoimmunity: When Defence Turns on You — interactive animation
• Inside the Beta Cell: How Insulin Is Released — interactive animation
• Nicotine: The Research
• Dr. Bryan Ardis on this subject — his claims, presented on their own pages and kept separate from this research collection
• The Nicotine Patch, animated
• Nicotinic Acetylcholine Receptors
• Cigarette Smoke — what burnt tobacco adds that nicotine alone does not
• Brain and Memory
• Mood and Mental Health
• Inflammation and Immunity
• Cancer Research
• Heart and Blood Vessels
• Metabolism and Weight
• Addiction and Withdrawal
• Patches, Gum and Delivery

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