Nicotine and Type II Diabetes

John (Gold)
John (Gold)

June 8th, 2004, 7:14 pm #1

Smoking May Boost
Diabetes Risk
Nicotine could be the culprit, increasing insulin resistance[/size]
By E.J. Mundell
HealthDay Reporter

MONDAY, June 7 (HealthDayNews) -- Smokers already worried  about their risks for cancer and heart disease now have another reason to quit: Tobacco may raise the risk for type 2 diabetes, say two new studies.

"This increased risk for type 2 diabetes could be due to increased insulin resistance, which has previously been shown to occur after an acute episode of smoking," said Dr. Valdemar Grill, a professor at both the University of Science and Technology in Trondheim, Norway, and the Karolinska Institute in Stockholm, Sweden.

He presented the findings of the first study on June 7 at the annual meeting of the American Diabetes Association (ADA) in Orlando, Fla. A second study presented by Johns Hopkins researchers at the meeting came to the same conclusion.

Experts have long understood that smoking does serious damage to arteries while raising risks for lung cancer. But studies are beginning to suggest it may encourage the development of diabetes, too.

In the latest study, Grill and his colleagues analyzed Norwegian government health data on nearly 39,000 adult men and women tracked over a period of 11 years.

They found that, regardless of gender, age, weight, physical activity and use of alcohol, smokers who smoked at least a pack of cigarettes a day faced a 64 percent higher risk of developing type 2 diabetes compared with nonsmokers.

The vast majority of diabetics -- about 95 percent -- are affected by type 2 diabetes, which develops when the pancreas fails to produce enough insulin to meet the body's demand or when body tissues become resistant to the effects of insulin. As insulin fails, blood sugar rises to unhealthy levels, raising the risks for cardiovascular disease and other health problems. Experts estimate that more than 18 million Americans have diabetes.

According to Grill, previous studies have suggested smoking contributes to insulin resistance. And since similar associations were found in people who used smokeless "snuff" tobacco, "it is likely that it is nicotine, the common substance in cigarettes and snuff, that is the culprit," he said.

"It is also possible that nicotine has a negative effect on insulin secretion," Grill added. "We have some data in animals to support this notion."

Curiously, the Norwegian study also found smoking was associated with lowered risks for two more rare forms of diabetes -- autoimmune diabetes (associated with dysfunction in the immune system), and type 1 diabetes. According to Grill, animal studies have suggested nicotine may actually help prevent the triggers behind autoimmune diabetes.

The risks far outweigh this potential minor benefit, however, and Grill strongly advises that all smokers "stop smoking because of the many proven and grave health hazards" associated with the habit.

Another study presented at the meeting seemed to back up the Norwegian findings. Researchers led by Dr. Hsin-Chieh Yeh of the Johns Hopkins School of Public Health examined data on nearly 9,000 older U.S. adults tracked for nine years.

They found that after adjusting for age, sex, race, weight and other factors, long-term smokers faced a 50 percent higher risk of developing diabetes compared with people who never smoked -- with risks rising as the number of years spent smoking increased.

Commenting on the two studies, Dr. Nathaniel Clark, the ADA's national vice president for clinical affairs, admitted he was "a little surprised" by the findings.

"When we usually list the risk factors for diabetes, smoking is never on that list. In that sense, this is new information," he said.

Although the findings are too preliminary to prompt any change in official ADA policy when it comes to preventing diabetes, Clark said quitting smoking should be a no-brainer.

"There are so many reasons not to smoke. I can't imagine that a fear of developing diabetes would trump dying from lung cancer, or any of the other terrible things smoking does," he said.

More information

For more on diabetes, visit the American Diabetes Association.

Copyright © 2004 ScoutNews, LLC. All rights reserved.
Last edited by John (Gold) on February 16th, 2011, 3:46 pm, edited 3 times in total.

John (Gold)
John (Gold)

November 9th, 2005, 12:10 pm #2

Diabetologia 2005 Nov 4;:1-6

Fetal and neonatal exposure to nicotine in Wistar rats results in increased beta cell apoptosis at birth and postnatal endocrine and metabolic changes associated with type 2 diabetes.

Gerstein HC.

Department of Obstetrics and Gynecology, McMaster University, Rm 3N52 HSC 1200 Main Street W., Hamilton, ON, Canada, L8N 3Z5, [][/url]

AIMS/HYPOTHESIS: Epidemiological studies report an increased risk of obesity and type 2 diabetes in children born to women who smoked during pregnancy. This study examines the effect of fetal and neonatal exposure to nicotine, the major addictive component of cigarettes, on postnatal growth, adiposity and glucose homeostasis.

METHODS: Female Wistar rats were given either saline (vehicle) or nicotine (1 mg kg(-1) day(-1)) during pregnancy and lactation. Serum and pancreas tissue were collected from the infant rats at birth. Postnatal growth was assessed weekly until the rats reached 26 weeks of age and glucose homeostasis was examined by OGTTs performed at 7 and 26 weeks of age.

RESULTS: Exposure to nicotine resulted in increased postnatal growth and adiposity. Nicotine exposure also resulted in dysglycaemia at 7 and 26 weeks of age. Serum insulin concentrations were decreased in the pups exposed to nicotine at birth. This was associated with increased beta cell apoptosis (pups of saline-treated mothers 8.81.21% apoptotic beta cells; pups of nicotine-treated mothers 27.83.1% apoptotic beta cells).

CONCLUSIONS/INTERPRETATION: Fetal and neonatal exposure to nicotine results in metabolic changes in the offspring that are consistent with obesity and type 2 diabetes. We propose that these metabolic changes may be a consequence of the initial insult to the beta cell during fetal life and that this animal model has many characteristics of diabetes in humans.

PMID: 16270195


November 22nd, 2006, 7:50 am #3

Holy Mackerel!!! If I had known this one fact about smoking there is a good chance I might never have started smoking. The reason is that I knew I was at high risk for diabetes due to a very strong family history of diabetes.

What I am wondering now is, is there any evidence of reduced risk for diabetes in ex-smokers, and is there any evidence of improvement in diabetics who quit smoking?

5 days


November 22nd, 2006, 7:56 am #4

Often when people quit smoking they may find that medications that were adjusted for them while smoking may be altered in effectiveness once quitting. People on hypertensives, thyroid, depression, blood sugar drugs, and others may need to get re-evaluated for proper dosages once quitting.

The first few days quitting can be very difficult to determine, what is a "normal" withdrawal and what is a medication dosage issue. But once through the first few days, if a person who is on medications for medical disorders finds him or herself having physical symptoms that just seem out of the ordinary, he or she should speak to the doctor who has him or her on the medications. Point out to the doctor that you have recently quit smoking and started to notice the specific symptoms just after quitting and that they haven't improved over time. The doctor should know the medication and potential interaction that not smoking may be adjusting for and which way the dosing may need to altered.

Treating many conditions is a partnership between you and your physician. The doctor needs your input to effectiveness of any treatment, whether it be by physical measurements or by verbally communicating how you feel while under treatment. The treatment for one condition though is your primary responsibility. The condition--nicotine addiction. It is by no means a minor medical issue, it is in fact probably the greatest controlable health threat anyone will ever face. Afterall, what other lifestyle issues carry a 50% premature mortality rate? Not to mention all the other crippling side effects that go along with long-term smoking. The treatment for this condition is your primary responsibility. To effectively treat smoking for the rest of your life simply remember to never take another puff!



November 22nd, 2006, 8:01 am #5

People with diabetes are at risk for a host of medical problems. High among them are risks of circulatory complications. Smoking too exacerbates risks of cardiovascular, cerebrovascular and peripheral vascular illnesses and complications. People who are diabetic and smoke are dealing with synergistic risk factors. Here are links to articles that discuss these implications:

Circulation / blood flow - how each new puff impairs oxygen delivery

New video covering the issues in this string:

High resolution version for Broadband connections:

Dial up version:
2.81 MB

19 minutes, 18 seconds long


July 11th, 2009, 4:09 am #6

Smoking as an independent risk factor for myocardial infarction or stroke in type 2 diabetes: a report from the Swedish National Diabetes Register

Eur J Cardiovasc Prev Rehabil. 2009 Jun 24. [Epub ahead of print]

Nilsson PM, Cederholm J, Eeg-Olofsson K, Eliasson B, Zethelius B, Fagard R, Gudbjörnsdóttir S; for the Swedish National Diabetes Register.
aDepartment of Clinical Sciences, Lund University, University Hospital, Malmö bFamily Medicine and Clinical Epidemiology Section cGeriatrics Section, Department of Public Health and Caring Sciences, Uppsala University, Uppsala dDepartment of Medicine, Sahlgrenska University Hospital, University of Gothenburg, Gothenburg, Sweden eHypertension and Cardiovascular Rehabilitation Unit, Faculty of Medicine, University of Leuven, KU Leuven, Belgium.


BACKGROUND: Few earlier studies have analysed smoking as a risk factor for myocardial infarction (MI) or stroke in type 2 diabetic patients.

DESIGN AND METHODS: A longitudinal study involved 13 087 female and male patients with type 2 diabetes from the Swedish National Diabetes Register with no previous MI or stroke at baseline, aged 30-74 years, and with data available for all analysed variables, followed up for mean 5.7 years.

RESULTS: Adjusted hazard ratios (HRs) for smoking and first-incident fatal/nonfatal MI, stroke and total mortality were 1.7 [95% confidence interval (CI): 1.4-2.0; P<0.001], 1.3 (95% CI: 1.1-1.6; P = 0.006) and 1.8 (95% CI: 1.5-2.2; P<0.001), respectively, by Cox regression analysis, adjusted for age, sex, diabetes duration, hypoglycaemic treatment, haemoglobin A1c, blood pressure, body mass index, microalbuminuria, antihypertensive and lipid-lowering drugs. Adjusted HR was higher for fatal MI, 2.1 (95% CI: 1.7-2.7; P<0.001), than for nonfatal MI, 1.4 (95% CI: 1.2-1.7; P<0.001). The highest HRs were observed in more frequently smoking (22%), middle-aged patients (age <60 years) for fatal/nonfatal MI, 2.3 (95% CI: 1.8-3.1; P<0.001) and for total mortality, 2.5 (95% CI: 1.6-3.8, P<0.001), whereas lower HRs were observed in older and less smoking patients. With predicted cessation of smoking in patients aged below 60 years, 24% (95% CI: 15-33%) of cases of fatal/nonfatal MI and 24% (11-37%) of cases of total mortality may have been prevented.

CONCLUSION: The risk for MI and total mortality associated with smoking is high in type 2 diabetes, especially in more frequently smoking, middle-aged patients, and was higher for MI than for stroke, and also higher for fatal than for nonfatal events. Smoking cessation would strongly affect risk reduction.

Last edited by FreedomNicotine on January 5th, 2010, 4:11 pm, edited 1 time in total.

Joined: November 11th, 2008, 7:22 pm

January 5th, 2010, 4:09 pm #7

Diabetes risk elevated
short-term upon cessation
The below study could not have been released at a worse time (the New Year's quitting rush), as outrageous news stories have taken its findings totally out of context. Headlines and leads in a number of stories suggest to still challenged new quitters that quitting smoking can cause diabetes. Let's get to the meat of this and fast.

FACT: This study found that ex-smokers have a lower risk of diabetes (22%) than current smokers (31%). This study focused on new quitters, where under this study's diabetes definition there was a temporary risk increase to 73%.

Yes, the average quitter does experience temporary cessation weight gain which does alter blood sugar levels and temporarily elevate diabetes risk. This study relied heavily upon post cessation blood sugar levels in diagnosing RISK of diabetes. To quote from the full text of the study:

[font=&AMP]"We classified persons as having diabetes if they met any of the following criteria, adapted from the 1997 American Diabetes Association criteria: fasting glucose level of at least 7.0 mmol/L (126 mg/dL); nonfasting glucose level of at least 11.1 mmol/L (200 mg/L); current use of diabetes medication; or a positive response to the question, "Has a doctor ever told you that you had diabetes (sugar in the blood)?" In the primary analysis based on fasting glucose level and self-report, fasting glucose level was available for more than 95% of participants at each of the 4 clinic visits (1987 to 1998), regardless of smoking status. According to customary practice, persons who met criteria for diabetes on a single occasion were considered to have diabetes for the remainder of follow-up, regardless of subsequent changes in interview responses or glucose level."[/font]
[font=&AMP]As you can see, the study didn't examine treatment or severity but only diagnoses. But even using the above definition of diabetes, researchers found that:

[font=&AMP]"In a 9-year follow-up of 10 892 adults with no diabetes at baseline, those who smoked had a higher risk for diabetes than those who never smoked (hazard ratio, 1.42 [95% CI, 1.20 to 1.67]). Among smokers who quit, diabetes risk was highest within 3 years of quitting, was mediated by weight gain, and decreased to no excess risk by 12 years."[/font]
[font=&AMP]Yes, if we use food as a dopamine "aaah" replacement crutch for nicotine we can develop diabetes. Yes, if a former pack-a-day smoker becomes a couch potato during the 100 minutes per day (assuming 5 minutes per cig) they would have devoted to finding and smoking their daily allotment of smokes they may see weight gain.

Cessation weight gain does not need to occur and certainly doesn't need to be significant. But even if it does we know from this study and others that cessation weight gain is temporary and eventually we each climb from the smoker/quitter ditch to lose the pounds and diminish diabetes risk below that of continuing smokers (which remains 40% greater than that of a non-smoker).

Let's look at this one more way. Regardless of how calculated, the risk of death associated with continued smoking vastly exceeds diabetes death risks. For example, in 1998 there were 64,751 U.S. diabetes deaths and that includes never-smokers, smokers and ex-smokers. That same year there were 418,690 smoking related deaths.

Although totally avoidable if that be our desire, a few extra temporary pounds probably won't to kill us. Don't let this study be used to fuel deadly junkie thinking that putting up to 81 cancer causing chemicals and scores of toxins into our body is safer. It's insane! Still just one rule for each of us ... no nicotine today!

Breathe deep, hug hard, live long,

John (Gold x10)


Smoking, Smoking Cessation, and Risk for Type 2 Diabetes Mellitus
[font=&AMP]A Cohort Study[/font] [font=&AMP]Annals of Internal Medicine[/font]

[font=&AMP]January 5, 2010 vol. 152[/font] [font=&AMP]no. 1[/font] [font=&AMP]10-17[/font]

[font=&AMP]Hsin-Chieh Yeh[/font][font=&AMP], PhD[/font][font=&AMP]; Bruce B. Duncan, MD, PhD; Maria Inês Schmidt, PhD; Nae-Yuh Wang, PhD; and Frederick L. Brancati, MD, MHS[/font]


[font=&AMP]Background:[/font] [font=&AMP]Cigarette smoking is an established predictor of incident type 2 diabetes mellitus, but the effects of smoking cessation on diabetes risk are unknown.[/font]

[font=&AMP]Objective:[/font] [font=&AMP]To test the hypothesis that smoking cessation increases diabetes risk in the short term, possibly owing to cessation-related weight gain.[/font]

[font=&AMP]Design:[/font] [font=&AMP]Prospective cohort study.[/font]

[font=&AMP]Setting:[/font] [font=&AMP]The ARIC (Atherosclerosis Risk in Communities) Study.[/font]

[font=&AMP]Patients:[/font] [font=&AMP]10 892 middle-aged adults who initially did not have diabetes in 1987 to 1989.[/font]

[font=&AMP]Measurements:[/font] [font=&AMP]Smoking was assessed by interview at baseline and at subsequent follow-up. Incident diabetes was ascertained by fasting glucose assays through 1998 and self-report of physician diagnosis or use of diabetes medications through 2004.[/font]

[font=&AMP]Results:[/font] [font=&AMP]During 9 years of follow-up, 1254 adults developed type 2 diabetes. Compared with adults who never smoked, the adjusted hazard ratio of incident diabetes in the highest tertile of pack-years was 1.42 (95% CI, 1.20 to 1.67). In the first 3 years of follow-up, 380 adults quit smoking. After adjustment for age, race, sex, education, adiposity, physical activity, lipid levels, blood pressure, and ARIC Study center, compared with adults who never smoked, the hazard ratios of diabetes among former smokers, new quitters, and continuing smokers were 1.22 (CI, 0.99 to 1.50), 1.73 (CI, 1.19 to 2.53), and 1.31 (CI, 1.04 to 1.65), respectively. Further adjustment for weight change and leukocyte count attenuated these risks substantially. In an analysis of long-term risk after quitting, the highest risk occurred in the first 3 years (hazard ratio, 1.91 [CI, 1.19 to 3.05]), then gradually decreased to 0 at 12 years.[/font]

[font=&AMP]Limitation:[/font] [font=&AMP]Residual confounding is possible even with meticulous adjustment for established diabetes risk factors.[/font]

[font=&AMP]Conclusion:[/font] [font=&AMP]Cigarette smoking predicts incident type 2 diabetes, but smoking cessation leads to higher short-term risk. For smokers at risk for diabetes, smoking cessation should be coupled with strategies for diabetes prevention and early detection.[/font]

[font=&AMP]Online study link:
Last edited by JohnPolito on January 5th, 2010, 4:20 pm, edited 2 times in total.

Joined: November 11th, 2008, 7:22 pm

February 16th, 2011, 3:47 pm #8

Nicotine and Type 2 Diabetes Journal:  Toxicological Sciences      

Source Link:

Authors:   Joseph L. Borowitz1 and Gary E. Isom

Author Affiliations:   Neurotoxicology Laboratory, Department of Medicinal Chemistry and Molecular Pharmacology, College of Pharmacy, Purdue University, West Lafayette, IN

To whom correspondence should be addressed. Fax: (765) 494-1414. E-mail: [][/url].

Received February 26, 2008.     Accepted March 4, 2008.

There are nearly 20 million type 2 diabetics in the United States. This common disease is characterized by a gradual decline in pancreatic insulin secretion and worsening hyperglycemia. There are many good drugs for treating type 2 diabetes but normal blood glucose levels are difficult to maintain. Hyperglycemia is especially detrimental since high glucose nonenzymatically cross links blood vessel proteins throughout the body, thickens vascular lumina, and interferes with endothelial function. Any kind of peripheral vascular problem would be accentuated by hyperglycemia.

Type 2 diabetes is often part of the “metabolic syndrome” characterized by obesity, hypertension, high blood lipids, and resistance to insulin. The metabolic syndrome affects about 25% of the population and is increasing worldwide with the increase in obesity. The hypertension and high blood lipids which often occur with diabetes further stress vessels in the presence of hyperglycemia. These disease states combined with coronary heart disease give rise to much morbidity and mortality and are leading causes of death in industrialized nations.

Since fetal development is so rapid, it is not surprising that chemicals can damage the fetus. Because type 2 diabetes may begin in utero, it is important to understand processes involved in formation of the endocrine pancreas. Endocrine cells arise from pancreatic progenitor cells during embryogenesis. These progenitor cells receive many signals, some mitogenic and some for differentiation (Dhawan et al., 2007). Progenitor cells persist throughout embryogenesis, but in the early postnatal period, high rates of beta cell proliferation cause a large increase in endocrine cells. Although beta cell mass expansion is slow in adults, pregnancy or obesity can cause hyperplasia and increased insulin synthesis/secretion (Dhawan et al., 2007). Existence of progenitor cells in the adult pancreas is controversial, but Xu et al. (2008) report that progenitor cells can be activated in injured adult mouse pancreas and are located in the ductal lining. They show expression of neurogenin-3, the earliest islet cell transcription factor, in the injured pancreas. Thus, not only are fetal tissues at risk but also beta cell proliferation, in the early postnatal period and perhaps in later periods, may be sensitive to chemical damage.

Despite the known vulnerability of fetal cells, chemical exposure and damage occurs. About 15–20% of all women smoke during pregnancy (Andres and Day, 2000). Epidemiological studies show a relationship between smoking and hypertension, type 2 diabetes, and obesity in the adult offspring of smoking mothers (Montgomery and Ekbom, 2002; Von et al., 2002; Wideroe et al., 2003). Such deliberate use of toxic substances which cause damage to developing humans, places a large financial burden on our medical care program.

Nicotine replacement therapy is recommended to pregnant women in Canada as a safe aid for breaking the smoking habit. Yet, Holloway et al. (2005) report that rats exposed to nicotine during gestation and lactation (PND21) show apoptosis of insulin-secreting cells. Increased postnatal weight with adiposity was also noted during the first 26 weeks of age. Both at 7 and 26 weeks, these nicotine-exposed animals show abnormal glucose tolerance. Holloway et al. (2005) concluded that fetal and neonatal exposure to nicotine in amounts comparable to those of human exposure causes a syndrome in rats similar to human type 2 diabetes.

Bruin et al. (2007) found that beta cell mass is decreased by about 25% following nicotine exposure either in utero or after both fetal and neonatal exposure. However, those animals not exposed during lactation, recover beta cell mass by 26 weeks, whereas those exposed both in utero and during lactation do not. It appears that nicotine can destroy those cells responsible for beta cell regeneration if it is present both during pregnancy and lactation. Elevated and prolonged blood glucose was also seen in response to an oral glucose challenge at 26 weeks but only in offspring exposed to nicotine for the entire fetal and neonatal period. Thus, two different cell processes may be affected by nicotine. One, beta cell proliferation and the other, beta cell apoptosis. Nicotine must be given for a longer period of time in order to affect cell proliferation.

In the paper highlighted in the present issue, Bruin et al. (2008) further extended the studies of Holloway et al. (2005) and elucidated some mechanisms by which nicotine increased beta cell apoptosis. Number of mitochondria decreased about 13% in beta cells from nicotine-exposed subjects and the remaining mitochondria were swollen so that they were about 50% larger than in saline controls and most likely dysfunctional. Changes in proteins regulating apoptotic cell death were also noted. Bcl-2 decreased in cytoplasm and allowed Bax to attach to mitochondria. Bax opened the mitochondrial permeability transition pore to release cytochrome c into the cytosol. Cytochrome c formed an apoptosome and activated caspase 3, the executioner protease responsible for the apoptotic changes and cell death. Bruin et al. (2008) concluded that nicotine exposure during pregnancy and lactation increased beta cell apoptosis in the offspring by the mitochondrial pathway.

Nicotine-induced apoptosis of beta cells may be mediated through nicotinic receptors. Yoshikawa et al. (2005) demonstrated specific binding of [3H] nicotine to beta cells and showed that nicotine inhibits glucose- as well as tolbutamide-induced insulin release from isolated rat and human islets. However, nicotine given iv actually releases insulin in mice if the effect of adrenal epinephrine is eliminated by adrenalectomy (Karlsson and Ahren, 1998. Ganglionic actions may overcome any direct effect of nicotine on pancreatic beta cells.

Nicotine need not act on surface nicotinic receptors. It is lipid soluble enough to penetrate into cells. Being an alkaloid, it is basic and would tend to collect in the relatively acidic intracellular environment. Also intracellular organelles like endoplasmic reticulum or secretory granules have a pH of about 4, so nicotine would concentrate further inside these compartments. It is not surprising that nicotine inhibits release of insulin from isolated islets.

Bcl-2 protein decreased in beta cells of nicotine-exposed pancreas to initiate the process of apoptosis. Since Bcl-2 is a redox-sensitive factor (Voehringer and Meyn, 2000), it appears that prolonged treatment with nicotine causes oxidative stress. How this occurs and whether nicotinic receptors are involved is not known. The mitochondrial changes are subsequent to changes in Bcl-2 protein and therefore are probably not a direct action of nicotine on mitochondria.

The vascular endothelium is a primary site for pathological changes in type 2 diabetes both in islets themselves and throughout the rest of the body. In fact, islets may be more sensitive than other tissues to changes in vascular endothelium. Not only do islets have five times more capillaries but also the endothelial lining shows 10 times more fenestrations than acinar tissue. Furthermore, the endothelium can affect adult beta cell function, promote beta cell proliferation, produce vasoactive and angiogenic substances, and growth factors. The islet microendothelium also fine-tunes blood glucose control (Zanone et al., 2008). Vasoconstrictors like nicotine and angiotensin II probably have more important effects on circulation to beta cells than to other cells of the body. Macfarlane et al. (2008) state that many clinical studies show drugs which block angiotensin II reduce the incidence of diabetes and may do so, in part, by improving islet function.

Once nicotine-induced damage to beta cells begins and type 2 diabetes develops, other mechanisms come into play. High glucose itself causes oxidative stress in beta cells (Robertson et al., 2007) and leads to progressive loss of function. High blood lipids also cause a loss of beta cell function (Hull et al., 2005). Associated deterioration of the vascular endothelium with reduced vascular flexibility in type 2 diabetes results in increased pulse pressure and pulse wave velocity and also shear stress (Cameron and Cruickshank, 2007). Impaired nitric oxide production is part of vascular stiffening (Soucy et al., 2006), and type 2 diabetics lack the powerful vasodilating action of nitric oxide so that deterioration of tissue perfusion occurs throughout the body. Continued exposure to the vasoconstrictor nicotine would further exacerbate the problem. To counteract blood vessel stiffening, Sharma (2007) suggests that drugs which block phosphodiesterase be used so that accumulation of cyclic GMP would occur in endothelial cells releasing nitric oxide to promote profound vasodilation. These nitric oxide generators may relieve endothelial dysfunction in type 2 diabetes.

Much effort and money have been spent developing drugs for treatment of type 2 diabetes. The sulfonylureas have been used for about 50 years, and the meglitinides are even more effective and actually enhance glucose-induced insulin release. They also have a shorter duration of action and cause less hypoglycemia. Metformin is even better and causes no hypoglycemia or obesity and reduces stroke and heart attacks in these patients. Many of these antidiabetic drugs give rise to obesity, and the elevated blood lipids may explain why beta cell function deteriorates when these drugs are used. The significance of the highlighted paper is that it provides mechanistic data on the adverse effects of nicotine on the developing pancreas and suggests that another way to approach the type 2 diabetes problem would be to avoid exposure of the fetus and neonate to nicotine.

As alcohol has some specificity for brain cells (corpus callosum, cerebellum, and frontal cortex) in fetal alcohol syndrome (FAS), nicotine appears to have a specificity for beta cells of the pancreas. It was thought that the incidence of FAS was about 0.1% of the population, but now we know the incidence is 1%. It is the number one cause of mental retardation in the United States and yet is 100% preventable. The severe form of FAS with nasal hypoplasia, droopy eyelids, and poor coordination is rare but more subtle changes occur at lower doses. Even when no physical abnormalities are apparent, behavioral changes can occur. Some FAS patients may have a normal IQ but at the same time may have impaired ability to relate to other people and are not able to use their intelligence. Similarly, low doses of nicotine during pregnancy and lactation may cause more subtle changes in pancreatic beta cell function and glycemic control. Publications by Holloway et al. (2005) and Bruin et al. (2007, 2008) have highlighted the fact that nicotine destroys insulin-secreting cells in the pancreas, and these authors have exposed a major clinical toxicology problem. Beta cells of the pancreas are susceptible to the toxic action of nicotine both during gestation and in the neonatal period. Dysglycemia occurs in the offspring of nicotine-treated rats when they are challenged with glucose as young adults. These animals appear to have a form of type 2 diabetes. Nicotine in any form should be avoided during pregnancy and lactation.
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   [*]© The Author 2008. Published by Oxford University Press on behalf of the Society of Toxicology. All rights reserved. For Permissions, please email:
Last edited by JohnPolito on February 16th, 2011, 4:00 pm, edited 1 time in total.

Joined: November 11th, 2008, 7:22 pm

April 5th, 2011, 10:58 pm #9

A Prospective Study Investigating the Association Between Environmental Tobacco Smoke Exposure and the Incidence of Type 2 Diabetes in Never Smokers
Annals of Epidemiology,   Volume 21, Issue 1, January 2011, Pages 42-47
Available online 2 December 2010.
Kwang-Pil Ko MD, PhD, Haesook Min MS, Younjhin Ahn PhD, Seon-Joo Park Phd, Cheong-Sik Kim PhD, Jae Kyung Park MPH and Sung Soo Kim PhD
Purpose We studied a cohort of individuals to assess whether intensity of environmental tobacco smoke (ETS) exposure is associated with the incidence of type 2 diabetes.

Methods Study subjects were selected from an ongoing population-based cohort of Korea Genome and Epidemiology Study. Participants of the baseline study 10,038 persons within the age range of 40 to 69 years old. Among 4,442 never smokers without prevalent diabetes, 465 type 2 diabetes cases were identified through biennial active follow-ups for a 6-year period. Cox proportional hazard models were used to estimate the hazard ratio (HR) and 95% confidence intervals (CI) after adjustment for covariates.

Results The risk of type 2 diabetes was higher in subjects exposed to ETS compared with the nonexposure group (HR = 1.41, 95% CI: 1.1–1.70). Daily exposure to ETS at home increased the risk of type 2 diabetes when compared with the risk level of nonexposure (HR = 1.46, 95% CI: 1.16–1.83). Over 4 hours exposure to ETS at home and in the workplace was associated with increased the risk of type 2 diabetes (HR = 1.96, 95% CI: 1.21–3.19).

Conclusions Our study suggests that ETS exposure is a significant risk factor for the development of type 2 diabetes with dose-response relationship.