Important note: smoking may offer a limited degree of protection in some individuals against the development of a small number of diseases, outlined below. However, this information is of little relevance to public health, given that the amount of disease that tobacco may be said to prevent is insignificant in comparison with the far greater incidence of disease caused by smoking. Tobacco products kill one in two of their long-term users.
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However, the evidence that tobacco consumption can prevent lives being lost to these diseases and conditions is limited and further mechanistic studies are required for causal inference.
Further, the number of deaths that may be prevented by smoking pales into insignificance compared to the number of deaths it has been demonstrated to cause. It is estimated that in 2015–16 tobacco use prevented 79 deaths in Australia, a very low number compared to the 20,031 deaths caused by smoking in that same year.
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On the basis of these figures, tobacco might be said to save about one life for every 250 deaths it causes. Moreover, there is nothing to suggest that possible protection conferred against one disease will stop a given smoker from developing another tobacco-caused disease.
So, for example, an individual who may have avoided Parkinson’s disease due to his or her smoking still runs a significant risk of dying from heart disease, lung cancer, or any of the multiplicity of other tobacco-caused diseases. Equally, smoking does not prevent Parkinson’s disease in all smokers.
While tobacco use cannot in any way be recommended as a prophylactic for these diseases and conditions, research on the mechanisms by which smoking appears to confer a protective effect against development of certain disease processes may lead to therapeutic benefits
Tobacco use may confer a small degree of protection against a small number of diseases and conditions, described in the sections below.
1. Ulcerative colitis
Ulcerative colitis is a serious bowel disease in which the inner lining of the colon and rectum becomes inflamed and permanently damaged.
Current smokers have a lower risk of developing ulcerative colitis, compared to non-smokers and ex-smokers, and according to the US Surgeon General, the evidence suggests that this protective relationship may be causal.
A dose–response relationship has also been found, such that greater pack-years or numbers of cigarettes smoked per day were associated with a decreased risk of ulcerative colitis. Though, there is no evidence that smoking improves the disease outcomes of those with ulcerative colitis.
In addition, smokers have a greater risk of developing Crohn’s disease, another inflammatory disease of the bowel. Due to the devastating effects of tobacco use, smoking is not recommended as treatment for ulcerative colitis, even though one research study has canvassed this as an extreme possibility for ex-smokers with steroid-dependent and resistant ulcerative colitis.
Nicotine in tobacco smoke is thought to be the component that is most likely to affect the development of the disease.
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Various forms of nicotine therapy are being evaluated to assess any possible benefits for individuals with this bowel disease. A 2004 Cochran review found that nicotine patches could reduce flare remission of ulcerative colitis but they were not significantly better than standard medical treatment therapy and caused additional side-effects.
It is theorized that nicotine reduces the risk of ulcerative colitis by decreasing the production of pro-inflammatory interleukin and the concentration of ad reno corticotropic hormone and cortisol, or by mediating the anti-inflammatory effect by acting on alpha-7 nicotinic acetylcholine receptors.
2. Parkinson’s disease
An association between smoking and a lower incidence of Parkinson’s disease has been observed across cohort and case-controlled.
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According to pooled estimates from a meta-analysis of both cohort and case-controlled studies, current and former smokers have a 41% lower risk of Parkinson’s disease relative to never smokers (RR 0.59; 95% CI, 0.56-0.62).
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The study also found an inverse dose-response relationship, such that smoking for more than 30 pack-years was associated with a 61% reduced risk relative to never smokers (RR 0.39; 95% CI, 0.29–0.53).
Based on the average data from 2014-15 and 2015-16 we can derive theoretical estimates that about 65 deaths from Parkinson’s disease are prevented by smoking in Australia annually.
Nicotine is thought to be the chemical in tobacco smoke most likely to be implicated in this finding, though the evidence is mixed and there may be other factors involved.
Some research suggests that nicotine can improve compromised semantic processing in Parkinson’s disease, and also influence semantic processing in healthy older individuals; however, the 2014 US Surgeon General’s report found that controlled trials of the effects of nicotine on cognitive function in patients with Parkinson’s disease are limited, with inconsistent findings.
More recent research suggests that genetics may also play a role in the association between smoking and Parkinson’s disease. Separate studies have indicated that the presence of specific variants of the RXRA and SLC17A6 genes related to xenobiotics, and the MAO-B and HLA-DRB1 genes associated with Parkinson’s disease, may be affecting the association of smoking and reduced Parkinson’s risk.
3. Endometrial cancer and uterine fibroids
Epidemiological studies have consistently reported that active cigarette smoking is inversely associated with developing cancer of the endometrium (the membrane lining of the uterus) in women who have reached menopause.
A meta-analysis found that cigarette smoking was significantly associated with a reduced risk, especially so among postmenopausal women, where a 29% reduction in risk was found (RR 0.71; 95% CI, 0.65–0.78).Very similar results have been reported from studies conducted in Poland although the researchers emphasis that in postmenopausal women, obesity is an important modifier of the association between cigarette smoking and the risk of endometrial cancer.
The Polish researchers found that obese women showed the greatest risk reduction for current smoking (OR 0.47; 95% CI, 0.27–0.81), a finding that further underscores the need for caution in interpreting these ‘favourable effects’ of smoking, considering the toxic and carcinogenic effects of tobacco.
Women who smoke may also have a decreased risk for uterine fibroids and endometriosis, but the evidence for this is not conclusive.
Development of endometrial cancer is predominantly influenced by exposure to the hormone oestrogen, and the protection conferred by smoking is likely to be due to the ‘anti-oestrogenic‘ effect of chemicals in tobacco smoke.
This same interaction works to increase the risk among smokers of developing osteoporosis, and reaching menopause earlier than non-smokers.
Based on the average of data from 2014–15 and 2015–16 we can derive theoretical estimates that smoking may prevent the loss of about 16 lives from endometrial cancer in Australia annually.
However the numbers of lives saved through the prevention of endometrial cancer among smokers are negligible compared with the number of deaths due to other diseases caused by tobacco use, including cancer of the uterine cervix.
4. Pre-eclampsia (hypertension in pregnancy)
Pre-eclampsia is a potentially serious condition in pregnancy in which the woman develops high blood pressure, fluid retention and abnormal kidney function.
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Smokers are less likely to develop pre-eclampsia than non-smokers. A study using Swedish birth registry data on more than 600,000 births examined the effects of snuff use and cigarette smoking on pre-eclampsia risk and found that compared with non-tobacco users, light smokers experienced a one-third reduction in risk (OR 0.66; 95% CI, 0.61–0.71) and heavy smokers a halving of risk (OR 0.51; 95% CI, 0.44–0.58) with risk lower for term than preterm pre-eclampsia.
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A meta-analysis has also indicated that there is a significant negative association between smoking and pre-eclampsia even after adjustment for BMI, maternal age, child sex and comorbid conditions.
The Swedish study also found that tobacco combustion products rather than nicotine are the probable protective ingredients against pre-eclampsia in cigarette smoke and further concluded that it is smoking behaviour in the middle or late rather than in the beginning of pregnancy that seems to have the greatest effect on the risk of pre-eclampsia.
A potential mediator of these associations might be carbon monoxide (CO), as it has vasoprotective properties, and CO and CO-releasing molecules lower levels of a particular protein that is higher in women who develop preeclampsia (sFlt-1) and soluble endoglobin in in vitro cultures.
There is also a suggestion that pre-eclampsia may occur less frequently in smokers because smoking is associated with a greater likelihood of preterm birth as well as other complications.
As pre-eclampsia develops in the late stages of pregnancy, smokers are less likely to be exposed the pre-eclampsia risk period. A study has estimated that if studies controlled for the risk of pre-term birth and other biases the effect of smoking itself on pre-eclampsia risk may be non-significant.
In 2004, the US Surgeon General concluded that ‘the decreased risk of pre-eclampsia among smokers compared with non-smokers does not outweigh the adverse outcomes that can result from prenatal smoking.
These conclusions are underscored by findings from a case–control study conducted in Canada where notwithstanding a (non-significant) reduction in the risk of pre-eclampsia, persistent smoking was also associated with a 10-fold increase in the risk of low birthweight (OR 10.2; 95% CI, 2.49–41.8) and a four-fold increase in the risk of preterm birth (OR 3.59; 95% CI, 1.06–12.1).
5. Cognitive performance
A meta-analysis of research into the effects of nicotine and smoking on human cognitive performance found positive effects of nicotine or smoking on six domains: (i) fine motor, (ii) alerting attention-accuracy, (iii) response time (RT), (iv) orienting attention-RT, (v) short-term episodic memory-accuracy, and (vi) working memory-RT (effect size range = 0.16 to 0.44).
There is evidence that nicotine may stimulate immediate and sustained improvements in working memory, that nicotine replacement in smokers avoids cognitive impairment through direct pharmacological effects on brain neuronal activity, and that nicotine may improve prospective memory (the retrieval and implementation of a previously encoded intention).
Note however that smoking in the longer term has been associated with cognitive decline.
Nicotine receptor-based medications have been trialled for the treatment of cognitive impairments in Alzheimer’s disease, though results indicated that they did not significantly improve cognition and had added side effects.
6. Psychiatric symptoms
The prevalence of smoking is higher among people with psychiatric conditions.
The reasons for this are complex, and vary between individuals and disorders.
Smokers often perceive their smoking to be helpful in relieving or managing psychiatric symptoms, and many mental health workers have traditionally believed that quitting smoking will exacerbate mental illness.
However, recent evidence suggests that the reverse is true; quitting smoking actually improves mental health, mood, and quality of life, both among the general population and among people with a psychiatric disorder.
7. Thyroid cancer
Some studies have suggested that smoking may be associated with a reduced risk of developing thyroid cancer, particularly for women.
However, one study found smoking was only associated with reduced thyroid cancer in men and others have found no protective effect.
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A 2018 meta-analysis of studies concluded the association between thyroid cancer risk and smoking was inconsistent and that further research is required before a definitive statement can be made.
8 Skin cancer
Early evidence suggests a protective of effect of smoking for certain types of skin cancers.
A meta-analysis of cohort studies found that current smoking was associated with a slightly reduced risk of developing basal cell carcinoma (RR = 0.85, 95% CI 0.75-0.96) and malignant melanoma (RR = 0.72, 95% CI 0.64-0.82).
However, the study also found that smoking was associated with a moderately greater risk of developing squamous cell carcinoma (RR = 1.32, 95% CI 1.15-1.52).
The evidence for this effect is limited, and the mechanism behind the effect and evidence for a dose-response relationship are both yet to be determined.
9. Other possible health ‘benefits’
There is some evidence that smokers and users of smokeless tobacco are less likely to develop aphthous stomatitis (common mouth ulcers).
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One study found that the possible protective effect of smoking was only present when there was heavy cigarette smoking or smoking for long periods of time (>5 years) and no significant associations were found between intensity or duration of smoking and clinical severity of aphthous stomatitis lesions.
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Transient increased incidence of mouth ulcers is commonly reported by individuals on quitting smoking.
A few studies have found smokers have lower incidence of conditions affecting the immune system including celiac disease (a disorder in which eating gluten triggers an immune response in the body, causing inflammation and damage to the small intestine) and Sjögren's sicca (an autoimmune condition where the immune system attacks and damages secreting glands, leading to symptoms of dryness, most commonly in the eyes and mouth).
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A meta-analysis found smokers were less likely to develop acute altitude sickness compared to non-smokers (OR = 0.71, 95% CI 0.52-0.96, P = 0.03).
Resulting in a net total of 20,110 deaths attributable to smoking in 2015–16.
