Nicotine Treatment For Ulcerative Colitis
Because of the potentially positive effects of nicotine on UC, clinical trials have tested the effectiveness of nicotine as a treatment for UC in the form of nicotine enemas, nicotine patches, delayed-release nicotine pills, or nicotine gum.
Studies found that former smokers with active UC typically had some symptom improvement with added nicotine compared to taking a placebo. However, nonsmokers with active disease who tried nicotine treatments typically did not experience any relief and were more likely to have mild side effects such as nausea, light-headedness, headaches, sleep disturbances, and skin irritation if they used a patch.
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volume 12, Article number: 7665
Stopping Smoking Is Unlikely To Worsen Symptoms Of Ulcerative Colitis
This is a plain English summary of an original research article
Non-smokers and people who stop smoking after being diagnosed with ulcerative colitis are unlikely to have more flare-ups or other signs of worsening disease, compared with those who continue to smoke.
Smoking is linked to reduced rates of developing ulcerative colitis in some studies. Some patients also believe that smoking can also lessen the symptoms of the disease, although previous research about this has had conflicting results. This study indicates that smoking does not have a significant effect on the illness after diagnosis.
Researchers followed 6,754 UK adults diagnosed with ulcerative colitis for 12 years. They compared outcomes for former smokers, non-smokers and smokers, and for people who stopped smoking after diagnosis. After adjusting for other factors, they found similar rates of corticosteroid use, flare-ups, hospital admissions and colectomy , regardless of smoking status.
People with ulcerative colitis can be encouraged to stop smoking, for the usual health-related reasons.
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Nicotine Suppresses The Production Of Pro
There is no doubt that the net effect of cigarette smoking is pro-inflammatory primarily as a result of increased oxidative stress, which occurs when the amount of reactive oxygen species generated in cells exceeds the capacity of normal detoxification systems . Oxidative stress is one potential explanation for the enhanced DNA breaks in smokers . Thus, it has implications for understanding the mechanisms by which smoking induces organ damage. There is overwhelming medical and scientific consensus that cigarette smoking causes lung cancer, heart disease, emphysema, and other serious diseases in smokers. Cigarette smoke contains molecules that act as potent carcinogens , as well as a large amount of ROS forming substances such as catechol or hydroquinone. However, nicotine, while being the addictive agent, is often viewed as the least harmful of these compounds. In fact, nicotine exhibits anti-inflammatory properties in many systems .
Prevalence Of Smoking Between Ibd Patients And Their Matched Controls
The flowchart of IBD patient selection for the study was shown in Fig. . In total, 790 patients were diagnosed with IBD and ever admitted during the study period. Among them, the detailed smoking history of 700 IBD patients was available. These 700 IBD patients were enrolled, and their data were analyzed for determining the influence of smoking on outcomes. The median follow-up periods of UC and CD patients were 104 and 85 months, respectively. We included 2 different control groups for each compared group , paired according to sex, age and presence of comorbidities, to compare the prevalence of smoking between IBD patients and matched controls. Only 575 patients with complete information of comorbidities and aged from 12 to 64 years old were enrolled with the median follow up time as 100 and 92.5 months, respectively.
Figure 1Table 1 Clinical characteristics of patients with UC and matched controls.
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Clinical Studies With Transdermal Nicotine
In an open trial 16 patients with left-sided colitis receiving various types of therapies were given in addition nicotine 30 mg daily in transdermal patches for 4 weeks. The majority of patients reported clinical, endoscopic and histological improvement during nicotine administration . Further, anecdotal observations supported that preliminary report.
A multicentre, double-blind, placebo-controlled trial carried out in the United Kingdom showed in patients with ulcerative colitis who had been applying transdermal nicotine in addition to their ongoing therapy a significantly superior effect in terms of clinical and histological improvement . Complete resolution of symptoms was observed in 48.6% of cases with nicotine and only in 24.3% of cases with placebo . Similar results have been reported by a multicentre, controlled trial performed in the United States, where at 4 weeks 39% of patients who received transdermal nicotine reported clinical improvementas assessed by a 13-point disease activity index that measured stool frequency, rectal bleeding, endoscopic findings and a clinical global evaluationcompared with 9% of patients who received placebo .
Time Relationships Between Cessation Of Smoking And Onset Of Ulcerative Colitis
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Pathogenic Mechanisms Of Smoking On Uc Patients
The exact mechanisms of action of nicotine and smoking in UC patients is not well known . Tobacco smoke contains hundreds of different substances including nicotine, free radicals and carbon monoxide. It is suspected that the main metabolite responsible for the impact on the course of UC is nicotine, however there is no absolute proof of nicotine being the sole active moiety. In consequence, probably the mechanisms are diverse and considering that the pathogenesis of UC is only partially understood, any dissertation on their possible mechanisms can only be hypothetical.
How Does Smoking Affect Your Digestive Tract
While youâre less likely to have UC if you smoke, the habit hurts your gastrointestinal tract in other ways. Thatâs because chemicals in cigarette smoke, and the large amounts of pollution breathed in during smoking, can damage your bodyâs tissues.
If youâve smoked for more than 2 years, you may also have a higher risk of stomach issues, due to a lower stomach pH . Smoking can also change how your gut repairs itself.
These factors suggest that, while smoking may protect you from getting UC, it can increase your risks for other inflammatory diseases.
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Who Gets Ulcerative Colitis
Studies show that some people are more likely to develop ulcerative colitis based on their:
- Age: Ulcerative colitis can develop at any age, but the disease is more likely to develop in adolescents or young adults in their 20s and 30s.
- Gender and sex: Ulcerative colitis occurs equally among genders. However, those assigned female at birth often report worsening symptoms leading up to their menstrual period.
- Geographical location: Ulcerative colitis is more common in North America and areas with colder climates such as northern Europe. Prevalence is increasing in areas of India.
- Family history: About 10-25% of those with ulcerative colitis have a first-degree relative with inflammatory bowel disease .
- Ancestry: It was previously thought that ulcerative colitis was more common in the Ashkenazi Jewish population. However, that hypothesis is fading as scientists learn more about the disease.
What Are The Implications
The risks to health of tobacco smoking are well-known, and advice to all smokers remains that these risks outweigh any potential benefits.
This study did not find any evidence to support the theory that smoking can reduce disease activity in ulcerative colitis, or that smoking has benefits for people with ulcerative colitis.
People with ulcerative colitis who smoke can be encouraged to stop, without it influencing their colitis.
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Nicotine Might Be A Potential Treatment For Ucsomeday
Researchers are studying whether nicotine-replacement therapiesincluding gum, patches, and nicotine enemascan relieve UC symptoms in the same way smoking does. Although some people with UC report finding symptom relief from patches and gum, the science proving a benefit still isnt there. And right now, nicotine is not a recommended therapy for UC, Dr. Magier adds. He prescribes 5-aminosalicylic acid treatments , steroids, and anti-TNF injections instead.
What Goes Into The Body
A healthy intestine typically has a diverse microbiome and a healthy immune response. This balance can change based on genetics, diet, exercise, and what goes into your body.
Unhealthy foods, preservatives, and certain medications can affect the intestines. For example, some antibiotics can disrupt the microbiome in the gut .
While there is no evidence that food causes ulcerative colitis, certain foods can trigger symptoms. There is evidence that a plant-based diet decreases symptoms, while processed foods increase symptoms.
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Influence Of Smoking On Disease Course
Active tobacco smoking has a protective effect on the severity of UC the disease course is more benign in smokers than in non-smokers. Flare-up, hospitalization rates, the need for oral steroids and, more importantly, colectomy rate are reported to be lower in smokers compared with non-smokers, though this has not been observed in all studies.
The link between smoking and colectomy in UC patients is controversial. In a retrospective analysis of a large series of UC patients, current smoking was found to decrease the 10-year cumulative colectomy risk from 0.42 to 0.32. A subsequent meta-analysis with a total of 1489 UC patients found the risk for colectomy to be lower in current smokers compared with non-smokers.
In agreement with these results, a population-based cohort study performed in Europe with 771 UC patients prospectively included and followed for 10 years revealed a lower relapse rate in smokers compared with non-smokers. Another similar study carried out in the Netherlands by van der Heide et al with 295 UC patients identified smoking after diagnosis as a protective factor for colectomy , whereas pancolitis at diagnosis was a risk factor.
As well as the study by Beaugerie et al, Boyko et al reported a lower hospitalization rate in patients who were smoking at the onset of UC, but could not identify a difference in the colectomy rate between smokers and non-smokers.
Impact Of Cigarette Smoking On The Gastrointestinal Tract Inflammation: Opposing Effects In Crohns Disease And Ulcerative Colitis
- 1Millennium Institute on Immunology and Immunotherapy, Departamento de Genética Molecular y Microbiología, Facultad de Ciencias Biológicas, Pontificia Universidad Católica de Chile, Santiago, Chile
- 2Departamento de Gastroenterología, Facultad de Medicina, Pontificia Universidad Católica de Chile, Santiago, Chile
Cigarette smoking is a major risk factor for gastrointestinal disorders, such as peptic ulcer, Crohns disease , and several cancers. The mechanisms proposed to explain the role of smoking in these disorders include mucosal damage, changes in gut irrigation, and impaired mucosal immune response. Paradoxically, cigarette smoking is a protective factor for the development and progression of ulcerative colitis . UC and CD represent the two most important conditions of inflammatory bowel diseases, and share several clinical features. The opposite effects of smoking on these two conditions have been a topic of great interest in the last 30 years, and has not yet been clarified. In this review, we summarize the most important and well-understood effects of smoking in the gastrointestinal tract and particularly, in intestinal inflammation, discussing available studies that have addressed the causes that would explain the opposite effects of smoking in CD and UC.
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Mechanisms Of Action Of Nicotine
In spite of extensive investigation, the exact mechanisms involved in the therapeutic effects of nicotine in ulcerative colitis remain elusive. It has been reported that nicotine increases the thickness of colonic mucus, thus enhancing the protection of the intestinal mucosa , but this remains to be confirmed. A reduction in intestinal blood flow by nicotine has also been described , but it is unlikely that this phenomenon may account for the favourable effects of nicotine in ulcerative colitis, since rectal blood supply in ulcerative colitis patients is already lower than normal .
It has been suggested that nicotine influences the cellular and the humoral immune system and interferes with the inflammatory response, perhaps through stimulation of endogenous steroid release . Indeed nicotine has been found to suppress in vivo Th2 cell function as measured by inhibition of interleukin-10 production , and to reduce the synthesis of interleukin-2 and interleukin-8 by mononuclear cells.
Nicotine can affect gut motility , but the possible relevance of this effect to its activity in ulcerative colitis is unknown. Smoking appears to decrease intestinal permeability , but a similar effect by nicotine has not been demonstrated.
Why Was This Study Needed
Ulcerative colitis causes inflammation and ulceration of the colon and rectum. It is thought to affect about 1 in 420 people in the UK. Some observational studies have suggested that people who smoke are less likely to develop ulcerative colitis than people who do not smoke, or who used to smoke. It is unclear why this is.
Previous evidence looking at the effect of smoking on people with ulcerative colitis has been inconclusive. A meta-analysis of 16 studies from 2016 found no evidence that smoking reduced disease progression or flares. However, other studies which tended to focus on specialist services, did find an effect. Some people with ulcerative colitis believe smoking helps their symptoms and continue to smoke, for this reason, risking other poor health outcomes from tobacco use.
This study was designed to evaluate the effect of both smoking status and smoking cessation on disease outcomes for people with ulcerative colitis, treated in the community or specialist services.
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Smoking And Ulcerative Colitis
The initial observation in 1982 by Harries and colleagues, that ulcerative colitis was largely a disease of non-smokers was made almost by serendipity, when a population of patients with colitis were used as controls in a study of nutritional aspects of Crohn’s disease. Only 8% of 230 patients with colitis were current smokers compared with 44% of the matched controls. Since this initial observation, there have been many published case-control studies in different countries which have consistently identified the association. Although there are variations in the calculated relative risks, most of the case-control studies confirm that the relative risk of colitis in ex-smokers is greater than lifelong non-smokers, with a reduced risk in current smokers. In one study, which is representative of the literature, the relative risks in ex-smokers, non-smokers, and smokers were 2.5, 1.0, and 0.6, respectively, with a high figure of 4.4 for ex-smokers who smoked more than 11 cigarettes daily.
Nachr Agonists Worsen Colitis
Given the proposed role of the 7nAChR in mediating the effects of stimulation of cholinergic anti-inflammatory pathways, selective 7nAChR agonists may have more therapeutic potential in ameliorating colitis than nicotine. Snoek et al. explored the effects of nicotine and two selective 7nAChR agonists on disease severity in two mouse models of acute experimental colitis. Colitis was induced by administration of DSS in the drinking water or 2,4,6-trinitrobenzene sulphonic acid intrarectally. Nicotine, AR-R17779, or GSK1345038A was administered daily by i.p. injection. After 7 days clinical parameters and colonic inflammation were scored.
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Tolerability Of Transdermal Nicotine
Adverse effects during therapy with transdermal nicotine were significantly more frequent than with placebo in all three placebo-controlled trials . The side-effects most commonly observed with nicotine were nausea, light-headedness, headache, sleep disturbances and skin irritation. The number of nicotine side-effects was significantly higher even compared with prednisolone but it must be noted that the steroid was employed at a dose of only 15 mg daily. When administered in standard doses corticosteroids were no better tolerated than nicotine .
In general adverse reactions occurred much more frequently in lifelong non-smokers than in former smokers and tended to appear especially during the first 2 weeks of therapy . Treatment withdrawals because of nicotine side-effects ranged from 5.7 to 13% .
Although no clear correlation was found between nicotine plasma levels and incidence of adverse effects , it appears that daily doses of nicotine up to 15 mg are better tolerated .
On the whole transdermal nicotine treatment results in frequent side-effects, although most patients are able to complete the course of therapy. No withdrawal symptoms suggesting nicotine addiction have been reported either after 46 weeks of therapy in short-term studies, or after a period of up to 6 months in the only long-term study available . Clearly, alternative nicotine formulations able to minimize the adverse effects of nicotine patches are of interest.
Increased Severity Of Colitis In Mice Deficient In 7nachr
A major role of 7nAChR in colitis was demonstrated by the increased severity of colitis induced by dextran sulfate sodium in 7nAChR-deficient mice. 7nAChR-deficient mice lost significantly more body weight and had increased levels of proinflammatory cytokines in comparison to wild type mice as early as 3 days post-colitis . In addition, neither nicotine nor a selective 7nAChR agonist attenuated the degree of inflammation in 7nAChR-deficient mice. Nicotine has been found to reduce the LPS-stimulated production of TNF- and IL-1 from peripheral blood mononuclear cells from IBD patients . Thus, it is not surprising that excessive TNF- production as occurs in colitis can also be attenuated by activation of 7nAChR .
In isolated intestinal and peritoneal macrophages, nAChR activation enhanced endocytosis and phagocytosis and this effect induced a transiently enhanced mucosal passage of luminal bacteria, in agreement with the role of ACh in stress-induced epithelial permeability . The effect was mediated via stimulated recruitment of GTPase Dynamin-2 to the forming phagocytic cup and involved nAChR 4/2, rather than 7nAChR. However, despite enhanced luminal bacterial uptake, ACh reduced NF-B activation and pro-inflammatory cytokine production, while stimulating anti-inflammatory interleukin-10 production .
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