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Smoking, Smoking Cessation, and Risk for Type 2 Diabetes Mellitus: A Cohort Study

Hsin-Chieh Yeh, PhD; Bruce B. Duncan, MD, PhD; Maria Inês Schmidt, PhD; Nae-Yuh Wang, PhD; and Frederick L. Brancati, MD, MHS
[+] Article and Author Information

From The Johns Hopkins University, Baltimore, Maryland; Federal University of Rio Grande do Sul, Porto Alegre, Brazil; and University of North Carolina, Chapel Hill, North Carolina.

Acknowledgment: The authors thank the staff and participants in the ARIC Study for their important contributions.

Grant Support: The ARIC Study is supported by contracts from the NHLBI (N01-HC-55015, N01-HC-55016, N01-HC-55018, N01-HC-55019, N01-HC-55020, N01-HC-55021, and N01-HC-55022) and a grant from the NIDDK (5R01-DK56918-03).

Potential Conflicts of Interest:Grants received: H.C. Yeh (NIDDK), B.B. Duncan (Brazilian National Research Council), N.Y. Wang (NIDDK, National Center for Research Resources), F.L. Brancati (NIDDK).

Reproducible Research Statement:Study protocol: ARIC protocols are available in the public domain through the ARIC Web site (www.cscc.unc.edu/aric/). Statistical code: Not available. Data set: ARIC data are available through request from the NHLBI data repository.

Requests for Single Reprints: Hsin-Chieh Yeh, PhD, Welch Center for Prevention, Epidemiology, and Clinical Research, The Johns Hopkins University, 2024 East Monument Street, Suite 2-600, Baltimore, MD 21205; e-mail, hyeh1@jhmi.edu.

Current Author Addresses: Drs. Yeh and Brancati: Welch Center for Prevention, Epidemiology, and Clinical Research, The Johns Hopkins University, 2024 East Monument Street, Suite 2-600, Baltimore, MD 21205.

Drs. Duncan and Schmidt: Graduate Studies Program in Epidemiology, Federal University of Rio Grande do Sul, Avenida Luiz Manoel Gonzaga, 630/8, Porto Alegre, RS 90470-280, Brazil.

Dr. Wang: Welch Center for Prevention, Epidemiology, and Clinical Research, The Johns Hopkins University, 2024 East Monument Street, Suite 2-500. Baltimore, MD 21205.

Author Contributions: Conception and design: H.C. Yeh, B.B. Duncan, M.I. Schmidt, N.Y. Wang, F.L. Brancati.

Analysis and interpretation of the data: H.C. Yeh, B.B. Duncan, M.I. Schmidt, N.Y. Wang, F.L. Brancati.

Drafting of the article: H.C. Yeh.

Critical revision for important intellectual content: H.C. Yeh, B.B. Duncan, M.I. Schmidt, N.Y. Wang, F.L. Brancati.

Final approval of the article: H.C. Yeh, B.B. Duncan, M.I. Schmidt, N.Y. Wang, F.L. Brancati.

Statistical expertise: H.C. Yeh, N.Y. Wang.

Obtaining of funds: F.L. Brancati.

Administrative, technical, or logistic support: F.L. Brancati.

Collection and assembly of data: H.C. Yeh.

Ann Intern Med. 2010;152(1):10-17. doi:10.7326/0003-4819-152-1-201001050-00005
Text Size: A A A

Background: Cigarette smoking is an established predictor of incident type 2 diabetes mellitus, but the effects of smoking cessation on diabetes risk are unknown.

Objective: To test the hypothesis that smoking cessation increases diabetes risk in the short term, possibly owing to cessation-related weight gain.

Design: Prospective cohort study.

Setting: The ARIC (Atherosclerosis Risk in Communities) Study.

Patients: 10 892 middle-aged adults who initially did not have diabetes in 1987 to 1989.

Measurements: 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.

Results: 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.

Limitation: Residual confounding is possible even with meticulous adjustment for established diabetes risk factors.

Conclusion: 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.

Primary Funding Source: National Heart, Lung, and Blood Institute and National Institute of Diabetes and Digestive and Kidney Diseases.


Grahic Jump Location
Figure 1.
Study flow diagram.

Individuals may have met more than 1 exclusion criterion. ARIC = Atherosclerosis Risk in Communities.

Grahic Jump Location
Grahic Jump Location
Appendix Figure.
Nine-year adjusted hazard ratio for incident diabetes in 10 892 middle-aged adults, by tertile of pack-years of smoking at baseline.

Estimates are simultaneously adjusted for race, sex, Atherosclerosis Risk in Communities Study center, level of education, baseline age, body mass index, waist circumference, physical activity, triglyceride level, high-density lipoprotein cholesterol level, and systolic blood pressure. Bars indicate 95% CIs. Never-smokers are the reference group. Summary HRs were estimated in a model in which pack-years were handled as a continuous variable. HR = hazard ratio.

Grahic Jump Location
Grahic Jump Location
Figure 2.
Nine-year adjusted hazard ratio (1990–1998) for incident diabetes in 10 892 middle-aged adults, by years since quitting before baseline (1987–1989).

Estimates are simultaneously adjusted for race, sex, Atherosclerosis Risk in Communities Study center, level of education, baseline age, body mass index, waist circumference, physical activity, triglyceride level, high-density lipoprotein cholesterol level, and systolic blood pressure. Bars indicate 95% CIs. Never-smokers are the reference group.

Grahic Jump Location
Grahic Jump Location
Figure 3.
Adjusted hazard ratios for incident self-reported diabetes during 12 years in 10 406 middle-aged adults without diabetes at baseline and 3-year follow-up.

The circles connected by the solid line represent adults who quit smoking between baseline (1987–1989) and visit 2 (1990–1992). The squares connected by the dotted line represent smokers who continued to smoke. Nonsmokers are the reference group (not shown). Estimates are simultaneously adjusted for race, sex, Atherosclerosis Risk in Communities Study center, level of education, baseline age, body mass index, waist circumference, physical activity, triglyceride level, high-density lipoprotein cholesterol level, and systolic blood pressure. Bars indicate upper and lower CIs (for clarity, only one interval is shown for each estimate).

Grahic Jump Location




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Submit a Comment
Smoking alters DHEA levels and Type 2 Diabetes
Posted on January 5, 2010
James M. Howard
Conflict of Interest: None Declared

DHEA is low in diabetes. It is my hypothesis that all drugs of abuse cause a reciprocating reduction of DHEA which triggers a rebound of DHEA. I suggest this is the basis of addiction. Therefore, smoking triggers, periodically, an increase in DHEA which would function to counteract diabetes, periodically. When one quits smoking, therefore, this periodic increase in DHEA is stopped. Hence, diabetes is momentarily exacerbated.

Furthermore, I suggest this increased cycling of DHEA ultimately shortens the life span production of DHEA. Therefore, smoking is also connected with type 2 diabetes earlier than diabetes appears on average in nonsmokers.

Conflict of Interest:

None declared

Smoking Cessation as a Trigger for a Major Depressive Episode
Posted on January 11, 2010
Roy C. Ziegelstein
Johns Hopkins University School of Medicine, Johns Hopkins Bayview Medical Center
Conflict of Interest: None Declared

Yeh and colleagues (1) report that smoking cessation may increase the risk of developing type 2 diabetes, an observation that may be somewhat startling to both physicians and patients. This finding is perhaps not really that surprising given the well-known relationship between smoking cessation and weight gain that has been exploited by cigarette manufacturers for many years (2). Yeh and colleagues (1) found that weight gain did, in fact, explain some of the excess risk of incident diabetes in those who quit smoking. However, the mechanism of the increased risk of type 2 diabetes among those who stop smoking is undoubtedly more complex. In this regard, it is worth noting that smoking cessation can trigger a major depressive episode (3,4). An individual with a major depressive episode triggered by smoking cessation may be at risk for the development of type 2 diabetes as a result of being less attentive to healthy behaviors like following an optimal diet, taking prescribed medications or exercising. Depression is also associated with diminished insulin sensitivity among individuals at risk for type 2 diabetes mellitus (5). Furthermore, depression is associated with systemic inflammation (6) that may increase the risk of developing diabetes.

The article by Yeh and colleagues (1) should make physicians and patients more aware of the possibility that smoking cessation may increase the risk of developing diabetes. The period of time after an individual stops smoking may also be one in which he or she is more vulnerable to changes in mood that may have numerous effects on physical health and health risks. While Yeh and colleagues did not report on depression in the patients in their study, the development of a major depressive episode should be considered as a possible mechanism for the important observation they make regarding smoking cessation as a risk factor for the development of diabetes.


1.Yeh HC, Duncan BB, Schmidt MI, Wang NY, Brancati FL. Smoking, smoking cessation, and risk for type 2 diabetes mellitus: a cohort study. Ann Intern Med. 2010;152:10-17.

2.Boyd TC, Boyd CJ, Greenlee TB. A means to an end: slim hopes and cigarette advertising. Health Promot Pract. 2003;4:266-277.

3. Covey LS, Glassman AH, Stetner F. Major depression following smoking cessation. Am J Psychiatry. 1997;154:263-265.

4. Glassman AH, Covey LS, Stetner F, Rivelli S. Smoking cessation and the course of major depression: a follow-up study. Lancet. 2001;357:1929- 1932.

5. Wagner J, Allen NA, Swalley LM, Melkus GD, Whittemore R. Depression, depression treatment, and insulin sensitivity in adults at risk for type 2 diabetes. Diabetes Res Clin Pract. 2009;86:96-103.

6. Irwin MR, Miller AH. Depressive disorders and immunity: 20 years of progress and discovery. Brain Behav Immun. 2007;21:374-383.

Conflict of Interest:

None declared

Drug Cessation and Rebound Hyperphagia
Posted on January 15, 2010
Richard L. Shriner
University of Florida College of Medicine
Conflict of Interest: None Declared

We congratulate Yeh and colleagues for a job well done (1). Tonstad and colleagues had similar findings among patients with coronary heart disease: ex-smokers were more likely to have full metabolic syndrome and increased waist circumference (2). We have reported that tobacco and other drugs of abuse are associated with appetite suppression and discontinuation with hyperphagia and weight gain (3,4). Discontinuation of drug taking is so regularly associated with weight gain that most abstinence-oriented rehabilitation centers that detox and treat addicts have incorporated prophylactic diet and exercise into their programs. Drugs of abuse and food compete at the same brain reinforcement sites thus, cessation of an addictive substance can propel the patient to rebound hyperphagia and the rapid weight gain which is so highly associated with metabolic syndrome and diabetes (5).

It is unfortunate that data on eating habits were not available in the study by Yeh et al as frequencies of consumption as well as types of foods consumed are important variables. Many addiction professionals and self help groups teach that eating can soothe drug cravings and avoiding hunger is a helpful tactic to keep from "falling off the wagon". Thus, some recovering addicts carry sugar and many recovery meetings have cakes, cookies, and candies readily available. Indeed, some research using sugar placebos have found effects which augment smoking cessation recovery rates. Researchers support the idea that overconsumption of palatable foods (sweet, high salt and/or carbohydrate-rich) may be a sign of food addiction and another reason for the obesity problem and subsequent issues (6,7).

So as we move forward, patients contemplating cessation will likely need a comprehensive yet individualized program that includes checking of fasting blood glucose, fasting insulin (e.g. to calculate QUICK), C- reactive protein, behavioral and nutritional counseling (and for some pharmacotherapy) to ensure the removal of tobacco does not lead to overeating, weight gain, and increased risk of diabetes (8). For example, the usage of bupropion to mitigate the orexigenic effects of nicotine withdrawal (9).

It is also possible that the systemic inflammation (another risk factor for diabetes) that is supposedly reduced during smoking cessation may actually increase due to the rebound hyperphagia and/or a possible loss of beta 3 receptor adipocyte influence on thermogenesis during nicotine withdrawal, all resulting in rebound adiposity (10,11). More studies are needed to shed light on this issue.


1. Yeh HC, Duncan BB, Schmidt MI, Wang NY, Brancati FL. Smoking, smoking cessation, and risk for type 2 diabetes mellitus: A cohort study. Ann Int Med 2010; 152: 10-17.

2. Tonstad S, Svendsen M. Premature coronary heart disease, cigarette smoking, and the metabolic syndrome. Am J Cardiol 2005; 96:1681-1685.

3. Gamberino WC, Gold MS. Neurobiology of tobacco smoking and other addictive disorders. Psychiatr Clin North Am 1999; 22(2):301-12.

4. Hodgkins CC, Cahill KS, Seraphine AE, Frost-Pineda K, Gold MS. Adolescent drug addiction treatment and weight gain. J Addict Dis 2004; 23(3):55-65.

5. Gold MS, Graham NA, Cocores JA, Nixon SJ. Food Addiction? J Addict Med 2009; 3:42-5.

6. Cocores JA, Gold MS. The salted food addiction hypothesis may explain overeating and the obesity epidemic. Med Hypotheses 2009; 73(6):892-9.

7. Corsica JA, Pelchat ML. Food addiction: true or false? Curr Opin Gastroenterol 2009 Dec 29.

8. Corwin EJ, Klein LC. C-reactive protein and depressed mood in a sub-group of smokers during nicotine abstinence. Hum Psyhopharmacol 2003; 18(5):329-37.

9. Richmond R, Zwar N. Review of bupropion for smoking cessation. Drug Alcohol Rev 2003; 22(2):203-20.

10. Jessen AB, Toubro S, Astrup A. Effect of chewing gum containing nicotine and caffeine on energy expenditure and substrate utilization in men. Am J Clin Nutr 2003 Jun;77(6):1442-7.

11. Yarnell JW, Sweetnam, PM, Rogers S et al. Some long term effects of smoking on the haemostatic system: a report from the Caerphilly and Speedwell Collaborative Surveys. J Clin Pathol 1987; 40:909-13.

Conflict of Interest:

None declared

Diabetes, Risky Behaviors and Stress: Those Pesky Confounding Factors.
Posted on February 4, 2010
Jay R. Schrand
Conflict of Interest: None Declared

Diabetes, Risky Behaviors and Stress:

Those Pesky Confounding Factors.

Introduction - Background

Yeh et al report that smoking cessation slightly increases the risk for diabetes. They attribute this iatrogenic effect to the weight gain common after cessation(1). However, two important factors were not considered. Stress particularly during childhood(2) has strong graded effect on tobacco initiation and maintenance as well as obesity. Insular stroke(IS) was found to be related to smoking cessation(3). Because this relationship was observed in a convenience sample of the existing population, IS must play some role in the current tobacco cessation process.

Synthesis (Graphic)

Stress, through levels of cortisol, has an adverse effect on all major human sub-systems, but especially respiratory disorders and metabolic syndrome x (insulin resistance). Stress related depression is common to tobacco initiation(2), asthma(4), digestive disorders(5) and cardiovascular disease including stroke. Depressive symptoms are common in smoking cessation.

Nicotine a CNS and respiratory stimulant has been used to treat respiratory disorders including asthma. It increases respiratory drive, reducing hypoxia.

The insula translates internal and external senses into feelings to motivate action to achieve homeostatic balance. IS may disrupt the natural response to glucose and hypoxia levels, defeating self-medication efforts. However, in statistical studies, there would still be a correlation between reported smoking status and diabetes. We should not rule out the possibility that those who smoke are simply treating (self-medicating) stress related respiratory disorders.

Memories are malleable.

Studies of ACE's find that survivors of traumatic stress often lose autobiographic memory of details surrounding the event. The cessation process, often part of current mental health therapy entails changes in thought. Psychotherapy, group dynamics, hypnosis have been used to re-creating images and thoughts to foment a change in behavior. Imagine yourself as a nonsmoking (or thin) person. The population of interest, has had a high exposure to stress with an increased risk for tobacco use and obesity, and more likely exposed to memory changing influences. So, just how much credence can we give to self-reports of former or nonsmoking status?


As exquisite as the Yeh, Naqvi and ACE studies are by current standards, this demonstrates the difficulty trying to establish causality in human adaptive behavior. If A correlates with B, A may cause B, or C may be caused by a yet undiscovered factor C. Only when close attention to the temporal and specificity issues can relationships be considered causal. And, even then, some new undiscovered confounding factor may come to light.


1. Yeh HC, Duncan BB, Schmidt MI, Wang NY, Brancati FL.

Smoking, smoking cessation, and risk for type 2 diabetes mellitus: a cohort study.

Ann Intern Med. 2010 Jan 5;152(1):10-7.

2. Anda RF, Croft JB, Felitti VJ, Nordenberg D, Giles WH, Williamson DF, Giovino GA.

Adverse childhood experiences and smoking during adolescence and adulthood.

JAMA. 1999 Nov 3;282(17):1652-8.

3. Naqvi NH, Rudrauf D, Damasio H, Bechara A.

Damage to the insula disrupts addiction to cigarette smoking.

Science. 2007 Jan 26;315(5811):531-4.

4. Scott KM, Von Korff M, Alonso J, Angermeyer MC, Benjet C, Bruffaerts R, de

Girolamo G, Haro JM, Kessler RC, Kovess V, Ono Y, Ormel J, Posada-Villa J.

Childhood adversity, early-onset depressive/anxiety disorders, and adult-onset asthma.

Psychosom Med. 2008 Nov;70(9):1035-43.

5. Thomas C, Hyppönen E, Power C.

Obesity and type 2 diabetes risk in midadult life: the role of childhood adversity.

Pediatrics. 2008 May;121(5):e1240-9.

A graphic (flow chart) of the diabetes, smoking, & stress system can be viewed at:


Conflict of Interest:

In 1994, the author requested an educational grant from the Council for Tobacco Research to study the relationship between tobacco use and sleep apnea. This request was denied. However the letter seems to have become part of the tobacco archives: http://tobaccodocuments.org/ctr/60024574 4574.html. Aside from this, the author has no financial interest in the tobacco, diet, or health industries other than as a consumer of their products and services.

Is there an excess or lower diabetes risk in female cigarette smokers?
Posted on February 8, 2010
Altan Onat
Emeritus from Cerrahpasa Medical Faculty, Istanbul University, Turkey
Conflict of Interest: None Declared

Authors examining prospectively the association of smoking status with the development of incident type-2 diabetes in the ARIC cohort (1) arrived at the conclusion that smoking predicts incident diabetes, and smoking cessation leads to higher short-term risk. The first part of the conclusion was not convincing for several reasons: Firstly, because excess risk did not emerge in one-third (mild smokers) of the smokers.

Secondly, the study does not clarify whether this risk is valid only for men or for both sexes, since sex-stratified analyses are totally missing. In the regression analyses, the referent never smokers and the top tertile were composed predominantly of different sexes differing substantially in risk. Sex adjustment may not disclose the situation for women who may well have been unaffected by the habit, though adjusted combined analyses have yielded excess risk.

Thirdly, adjustment for body mass index (BMI) may be biased depending on whether or not smoking led to a reduction in obesity in this cohort. If it did, which seems to be so from the significantly lower BMI values noted in increasing categories of smoking, this would conceal a possible beneficial BMI-mediated effect of the habit to the risk of diabetes. This adjustment might introduce bias to male smokers as well.

Finally, compared with never smokers, the adjusted hazard ratio persisted to be slightly raised at least a decade after discontinuance and was reported to be increased 1.54-fold among those who had quit 3-5 years previously.

Despite the statement in the introduction that cigarette smoking is consistently identified as a risk factor for incident diabetes, the issue is far from established, and several studies (2,3) indicate smoking may partly protect (women) against diabetes. Indeed, in a part of the ARIC cohort, adjusted subjects with isolated impaired glucose tolerance, a prediabetic state more prone to diabetes, were less likely to smoke than those with normal or impaired fasting glucose (4). In most studies concerned, the group which subsequently developed diabetes had fewer smokers than those who did not develop. The D.E.S.I.R. study cited in authors' article offers convincing findings to explain these observations. Authors were right in considering the effect of smoking on the pro-inflammatory state mediating the development of diabetes. Yet a large meta -analysis on circulating CRP in over 160,000 participants (5), noted same or marginally lower CRP concentrations compared to non-smokers in female current smokers, though male current smokers had higher CRP levels. Thus the reader would appreciate to learn the effect of smoking in this study on the risk of diabetes in each sex without the mediation by BMI.

References 1. Yeh H-C, Duncan BB, Schmidt MI, Wang N-Y, Brancati FL. Smoking, smoking cessation, and risk for type 2 diabetes. Ann Intern Med 2010:152:1-17

2. Onat A, Ozhan H, Esen AM, Albayrak S, Karabulut A, Can G, Hergenc, G. Prospective epidemiologic evidence of a "protective" effect of smoking on metabolic syndrome and diabetes among Turkish women -without associated overall health benefit. Atherosclerosis 2007; 193:380-9

3. Nagaya T, Yoshida H, Takahashi H, Kawai M. Heavy smoking raises risk for type 2 diabetes mellitus in obese men; but, light smoking reduces the risk in lean men: a follow-up study in Japan. Ann Epidemiol 2008; 18:113-8

4. Pankow JS, Kwan DK, Duncan BB, Schmidt MI, Couper DJ, Golden S, Ballantyne CM. Cardiometabolic risk in impaired fasting glucose and impaired glucose tolerance: the Atherosclerosis Risk in Communities Study. Diabetes Care 2007; 30:325-331.

5. The Emerging Risk Factors Collaboration: C-reactive protein concentration and the risk of coronary heart disease, stroke and mortality: an individual participant meta-analysis. Lancet 2009 Epub Dec 22

Conflict of Interest:

None declared

Re:Smoking alters DHEA levels and Type 2 Diabetes
Posted on February 25, 2010
Hsin-Chieh Yeh
Johns Hopkins University
Conflict of Interest: None Declared

In Response: We agree with Dr. Ziegelstein that smoking cessation may trigger depression, which could in turn increase the risk of type 2 diabetes due to unhealthy behaviors, decreased insulin sensitivity, and/or increased systemic inflammation. Unfortunately, the ARIC Study did not include a specific assessment for depression. At the year 3 follow-up visit, ARIC participants were asked to complete a survey of 'vital exhaustion(1)thought to measure feelings of fatigue and exhaustion (scored on a scale of 0-42) that might precede myocardial infarction. As Dr. Ziegelstein suspected, vital exhaustion was greater in quitters than in never smokers (age-gender-race-ARIC center adjusted mean (SD): 11.3(9.3) vs. 9.1(8.3)), but adjustment for vital exhaustion did not appear to explain the higher risk of incident diabetes in quitters in the fully adjusted regression model.

Dr. Onat makes several interesting comments. First, he correctly points out that there was no excess risk for diabetes in smokers in the lowest tertile of cumulative pack-years (compared to never smokers). This 'lowest tertile group' was largely composed of former smokers (77%) who had likely quit over 10-15 years prior to enrollment in ARIC. Therefore, the results seem consistent with our finding that diabetes risk drifts down to the 'background rate' over this time interval. Second, he suggests that the common practice of introducing of BMI into multivariate models that relate smoking to diabetes risk might constitute inappropriate over-adjustment for a risk mediator (insofar as smoking-related weight loss might contribute to reduced diabetes risk) that would bias risk estimates upwards. We therefore conducted an additional analysis excluding BMI and waist circumference from the fully adjusted model. Removing BMI and weight circumference led to a small attenuation in the risk estimates, but the relationship remained graded and statistically significant. Third, he questions the appropriateness of pooling men and women into a single analysis, since the effects of smoking on weight might differ by sex. We therefore assessed for possible interactions in models with and without BMI and waist circumference. There was no evidence of effect modification by sex in either model. We therefore stand by our pooled approach.

Finally, Dr. Shriner's comments regarding potential changes in eating habits after quitting are well-taken. Unfortunately, we are unable to test his hypothesis in ARIC: the ARIC Study used a food frequency questionnaire (FFQ) to collect usual dietary intake, which does not reflect daily eating behavior per se, but rather long-term dietary patterns. Dr. Shriner also recommends fasting insulin and CRP as part of a post cessation monitoring plan. Although additional assays would provide further information, we do emphasize that demographic and clinical factors readily available in the primary care setting without extra cost appear to carry a great deal of predictive information: older men who were heavy smokers and gained more weight after quitting have by far the highest risk of developing diabetes. Physicians and patients should be aware of those risk factors even without additional blood assays.


1. Appels A, Hoppener P, Mulder P: A questionnaire to assess premonitory symptoms of myocardial infarction. Int J Cardiol 17:15-24, 1987

Conflict of Interest:

None declared

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Summary for Patients

Smoking, Quitting Smoking, and the Risk for Type 2 Diabetes

The summary below is from the full report titled “Smoking, Smoking Cessation, and the Risk for Type 2 Diabetes Mellitus. A Cohort Study.” It is in the 5 January 2010 issue of Annals of Internal Medicine (volume 152, pages 10-17). The authors are H.C. Yeh, B.B. Duncan, M.I. Schmidt, N.Y. Wang, and F.L. Brancati.


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