THE CONSULTANT | 79. Diabetes and Smoking a Bad Combination. There is great doubt that the increased cardiovascular burden of diabetes in combination ...
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Clinical Articles
FEATURE
Diabetes and Smoking a Bad Combination There is great doubt that the increased cardiovascular burden of diabetes in combination with smoking is fully appreciated by diabetics or communicated appropriately to diabetics by their carers, write Dr Zubair kabir and Prof luke Clancy
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he effects of smoking on mortality and morbidity from various diseases are well established and widely known. Among these, are vascular disease, cancer, COPD and asthma. Less well known to the general population but equally well established in the scientific literature are the effects of smoking on people with diabetes, both type 1 & 2. This article describes some of the causal, direct, and indirect effects of smoking on people with diabetes. It goes on to identify significant knowledge lacunae in relation to smoking and diabetes – viz, baseline information about smoking and diabetes is lacking; little is known about care provision and advice to diabetics who smoke; and little is known about initial and on-going education about diabetes, smoking and treatment of tobacco dependence to carers and makes recommendations regarding the types of information which should routinely be gathered. Finally, it draws attention to treatment of tobacco dependence as an effective, cost negative intervention, and urges such help for diabetic patients who smoke.
increaseD carDiOvascular risk It is well know that smoking is a major risk factor for ischaemic heart disease and cerebrovascular disease and peripheral vascular disease. These conditions are mainly due to macrovascular disease with the well-known controllable risk factors of smoking, hypertension, hyperlipidaemia, obesity, diabetes and physical activity. Control of these risk factors reduces the risk of dying of a heart attack or stroke. Micro-vascular disease is a significant feature of diabetes and the combination of vascular diseases is seriously deleterious. The direct role of smoking in diabetic microvascular complications is probable but not completely worked out. What seems much clearer and better established is that there is an increased risk of morbidity and earlier death associated with the development of macrovascular complications among smokers with diabetes. There is however great doubt that this increased cardiovascular burden of diabetes in combination with
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smoking is fully appreciated by diabetics or communicated appropriately to diabetics by their carers. Whether it is fully appreciated or taught to care providers themselves in training colleges is also uncertain. Wider Implications The role of smoking in the development of microvascular complications in diabetics has been studied and smoking is linked with its premature development. The results are increased likelihood of nephropathy, neuropathy and probably retinopathy although this is less scientifically secure. In total therefore according to Quitline Victoria, people with diabetes who smoke are more likely than non-smoking diabetics to: • Die from heart disease. • Suffer from circulation problems in their feet and legs, and develop blood vessel disease in the legs. • Have pain and need amputation of a limb due to blood vessel disease in the legs. • Develop life threatening kidney disease. • Have problems with movement and flexibility in the joints. • Develop nerve damage which can lead to numbness and pain. •Develop problems with getting or maintaining an erection, due to the effects of smoking on the blood vessels of the penis. •Develop gum disease which can lead to tooth loss. •Suffer eye damage. Increased risk of Infection in Diabetic Smokers While these vascular complications are most important and frequent complications of smoking in diabetics, smoking also poses other risks for diabetics. Infection is a serious complication in diabetes and smoking is a cause of increased susceptibility to infection. Mechanisms by which smoking increases the risk of infections are not fully understood but include structural changes in the respiratory tract and a decrease in immune response. However there is no doubt that cigarette smoking is a substantial risk factor for important bacterial and viral infections. It is believed that smokers have a 2- to 4-fold increased risk of invasive pneumococcal disease and in diabetics this will be exaggerated. Importantly influenza risk is several folds higher and is much more severe in smokers than nonsmokers. In recent years it has been recognised that the greatest public health impact of smoking on infection is the increased risk of tuberculosis which again has been traditionally regarded as an increased risk in diabetes especially where TB
is common. This increased infection risk due to smoking is seldom mentioned with regard to advising diabetics to stop smoking but may be a powerful tool as it is easy to understand how important it can be especially with regard to influenza. This infection risk also applies to secondhand smoke exposure which again is seldom explained to diabetics by their carers. It also increases the power of the message surrounding the advisability of vaccination for diabetics against pneumococcal and influenza disease. It would also justify the use of acyclovir treatment for varicella in smokers. The specific mechanisms by which cigarette smoking increases the risk of systemic infections are incompletely understood as mentioned but they are multifactorial and seem to be interactive in their effects. They include structural and immunological mechanisms which impair host defences. The structural damage done to the respiratory tract is well appreciated. The irritant components of smoke, of which there are many, include acrolein, acetaldehyde, formaldehyde, free radicals produced from chemical reactions within the cigarette smoke, and nitric oxide, may contribute to the observed structural alterations in the airway epithelial cells. The changes in the respiratory tract include peribronchiolar inflammation and fibrosis, increased mucosal permeability, impairment of the mucociliary clearance, changes in pathogen adherence, and disruption of the respiratory epithelium. These changes are thought to predispose to the development of upper and lower respiratory tract infections, which may amplify the cigarette smoke–induced lung inflammation particularly in diabetics. As regards the immune responses both cell-mediated and humoral-mediated mechanisms are involved. Polymorphonuclear (PMN) leucocyte counts are higher in smokers. There are also changes in lymphocytes. There are increased CD3+ and decreased CD4+ counts and a trend towards increased CD8+ lymphocyte counts. These changes may lead to an increased susceptibility to infection. Abnormal numbers of these cells are seen earlier in bronchoalveolar lavage fluid (BAL) than in blood suggesting a deficit in cellmediated immunity in the lung alveoli which is an important site for lung defence against infection. These changes in WCC are often accompanied by an increase in macrophages in BAL which also have a greater inhibitory effect on lymphocyte proliferation than macrophages from the lungs of nonsmokers. Since PMNs play a significant role in host defence against acute bacterial infections, an impairment of PMN functions
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Clinical Articles
by smoke may contribute to the increased susceptibility of smokers to systemic infections, including bacterial pneumonia. The effects of cigarette smoking on humoral immunity have been studied extensively. Several studies have found that smokers had serum immunoglobulin levels (IgA, IgG, and IgM) 10% to 20% lower than those of nonsmokers but they seem to increase following stopping. It is important to recognise and publicise that many of the immunologic abnormalities in smokers resolve within 6 weeks after smoking cessation, supporting the idea that smoking cessation is effective in a relatively short time in the prevention of infections. smOking as a cause Of DiabeTes Smoking is a recognised risk factor for causing Type2 diabetes (T2DM). A major review in 2007 showed that in 25 prospective cohort studies (N = 1.2 million participants) there were 45,844 incident cases of diabetes reported during a study follow-up period ranging from 5 to 30 years. The pooled adjusted relative risk RR was 1.44 (95% confidence interval [CI], 1.31-1.58). Results were consistent and statistically significant in all subgroups. The risk of diabetes was greater for heavy smokers (≥20 cigarettes/day; RR, 1.61; 95% CI, 1.43-1.80) than for lighter smokers (RR, 1.29; 95% CI, 1.131.48) and lower for former smokers (RR, 1.23; 95% CI, 1.141.33) compared with active smokers, consistent with a doseresponse phenomenon. This allowed the authors to conclude that active smoking is associated with an increased risk of type 2 diabetes. The mechanism seems linked with increased insulin resistance found in smokers. There is also a complex link between obesity, overweight, smoking and diabetes. smOking cessaTiOn fOr DiabeTic smOkers Despite decreases in smoking prevalence over time, people with diabetes are still as likely to smoke as those without diabetes. More than 40% of smokers with diabetes currently report never having received advice from a physician to quit smoking. Health care providers should increase their efforts to reduce smoking among people with diabetes. This occurs in the context of a common chronic condition which is increasing in incidence. The prevalence in Ireland is estimated to be already greater than 5% and likely to increase greatly in the next decade. While I stress the importance of increased smoking cessation services for patients with diabetes it is clear that the diabetic services in general need improving. To achieve this the Clinical Care and Strategy Directorate in the HSE established a National Diabetes Programme Working Group to examine how diabetes care is currently delivered to people with T2DM in Ireland and to see how diabetes care could be changed to ensure that people with T2DM receive the highest standard of medical care possible. This Integrated Model of Care for patients with Type 2 Diabetes is set to highlight the importance of smoking and smoking cessation. But how is that going to work? But have we the capacity to deliver a smoking cessation service to all these diabetic patients who smoke. Are all diabetic smokers going to be treated for tobacco dependence as part of their
FEATURE
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This allowed the authors to conclude that active smoking is associated with an increased risk of type 2 diabetes.” diabetic care? The HSE is rolling out instruction in brief intervention so everyone involved in diabetic care should have the basic knowledge to help patients stop smoking. hOw will inTervenTiOn impacT? Current knowledge suggests that brief intervention doubles success rate compared to no advice but that would still mean a small percentage of smokers quitting. This is not enough. Smoking cessation is not just a cost-effective intervention, it is cost-negative but it is likely that the vast majority of Irish healthcare professionals are not trained adequately to offer a state-of-the-art smoking cessation service. It is clear therefore that for integrated diabetic care to be effective in this regard it needs to relate to the existing smoking cessation services. Professionals trained in the mechanisms of tobacco dependence and the neurophysiology and neuropathology of nicotine and its related neuroactive substances are best placed to offer a rational and successful service to these patients. The psychological and pharmacological approaches to treatment of tobacco dependence have advanced greatly in the last decade so that we can now say that ‘cure rates’ of 20-30% are very achievable. This is probably unique among chronic relapsing diseases and certainly does not apply to T2DM or COPD or asthma or hypertension or hyperlipidaemia. It is difficult to understand our readiness to resource much less cost-effective interventions for other chronic diseases. I believe that at least part of the reason is that we have not acquired the necessary skills in medical, nursing or dental schools and advocate for what we feel best able to deliver to our patients with chronic disease. Many smokers stop unaided, others need encouragement through advice. But these approaches have low success rates when formally tested even though in surveys most people who stop have had to do so on their own, unaided. This is no longer necessary, counselling and pharmacotherapy separately or together have validated success rates several times greater than ‘cold turkey’. The health risks for diabetics from smoking are such that it is imperative that targeted cessation services are delivered and would yield huge gains in quality of life with reduction in cardiovascular and respiratory morbidity and mortality. The consequent health care cost savings would also be considerable. There can be no valid excuses for not implementing a smoking cessation service with these benefits to a patient group of great and increasing importance. Dr Zubair Kabir, Department of Epidemiology & Public Health, University College, Cork. Prof Luke Clancy, Tobacco Free Research Institute Ireland, Dublin
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