essay on smoking cessation

Essay on Smoking

500 words essay on smoking.

One of the most common problems we are facing in today’s world which is killing people is smoking. A lot of people pick up this habit because of stress , personal issues and more. In fact, some even begin showing it off. When someone smokes a cigarette, they not only hurt themselves but everyone around them. It has many ill-effects on the human body which we will go through in the essay on smoking.

Ill-Effects of Smoking

Tobacco can have a disastrous impact on our health. Nonetheless, people consume it daily for a long period of time till it’s too late. Nearly one billion people in the whole world smoke. It is a shocking figure as that 1 billion puts millions of people at risk along with themselves.

Cigarettes have a major impact on the lungs. Around a third of all cancer cases happen due to smoking. For instance, it can affect breathing and causes shortness of breath and coughing. Further, it also increases the risk of respiratory tract infection which ultimately reduces the quality of life.

In addition to these serious health consequences, smoking impacts the well-being of a person as well. It alters the sense of smell and taste. Further, it also reduces the ability to perform physical exercises.

It also hampers your physical appearances like giving yellow teeth and aged skin. You also get a greater risk of depression or anxiety . Smoking also affects our relationship with our family, friends and colleagues.

Most importantly, it is also an expensive habit. In other words, it entails heavy financial costs. Even though some people don’t have money to get by, they waste it on cigarettes because of their addiction.

How to Quit Smoking?

There are many ways through which one can quit smoking. The first one is preparing for the day when you will quit. It is not easy to quit a habit abruptly, so set a date to give yourself time to prepare mentally.

Further, you can also use NRTs for your nicotine dependence. They can reduce your craving and withdrawal symptoms. NRTs like skin patches, chewing gums, lozenges, nasal spray and inhalers can help greatly.

Moreover, you can also consider non-nicotine medications. They require a prescription so it is essential to talk to your doctor to get access to it. Most importantly, seek behavioural support. To tackle your dependence on nicotine, it is essential to get counselling services, self-materials or more to get through this phase.

One can also try alternative therapies if they want to try them. There is no harm in trying as long as you are determined to quit smoking. For instance, filters, smoking deterrents, e-cigarettes, acupuncture, cold laser therapy, yoga and more can work for some people.

Always remember that you cannot quit smoking instantly as it will be bad for you as well. Try cutting down on it and then slowly and steadily give it up altogether.

Get the huge list of more than 500 Essay Topics and Ideas

Conclusion of the Essay on Smoking

Thus, if anyone is a slave to cigarettes, it is essential for them to understand that it is never too late to stop smoking. With the help and a good action plan, anyone can quit it for good. Moreover, the benefits will be evident within a few days of quitting.

FAQ of Essay on Smoking

Question 1: What are the effects of smoking?

Answer 1: Smoking has major effects like cancer, heart disease, stroke, lung diseases, diabetes, and more. It also increases the risk for tuberculosis, certain eye diseases, and problems with the immune system .

Question 2: Why should we avoid smoking?

Answer 2: We must avoid smoking as it can lengthen your life expectancy. Moreover, by not smoking, you decrease your risk of disease which includes lung cancer, throat cancer, heart disease, high blood pressure, and more.

Customize your course in 30 seconds

Which class are you in.

Travelling Essay
Picnic Essay
Our Country Essay
My Parents Essay
Essay on Favourite Personality
Essay on Memorable Day of My Life
Essay on Knowledge is Power
Essay on Gurpurab
Essay on My Favourite Season
Essay on Types of Sports

Download the App

Essay on Stop Smoking

Students are often asked to write an essay on Stop Smoking in their schools and colleges. And if you’re also looking for the same, we have created 100-word, 250-word, and 500-word essays on the topic.

Let’s take a look…

100 Words Essay on Stop Smoking

Introduction.

Smoking is a dangerous habit that harms our health and environment. It’s crucial to stop smoking for a better life and future.

The Dangers of Smoking

Ways to quit.

You can stop smoking by seeking help from doctors, using nicotine patches, or joining support groups.

Benefits of Quitting

Quitting smoking improves health, saves money, and protects loved ones from secondhand smoke.

250 Words Essay on Stop Smoking

The detrimental effects of smoking.

Smoking is a habit that has been ingrained in numerous societies for centuries. Despite its prevalence, the deleterious effects of smoking on health are undeniable. Every puff of smoke inhaled introduces a cocktail of chemicals into the body, many of which are carcinogens. The result is a heightened risk of diseases such as lung cancer, heart disease, and stroke.

Smoking and Its Socioeconomic Impact

Beyond the health implications, smoking also presents significant socioeconomic challenges. The cost of tobacco products and healthcare for smoking-related illnesses can be financially crippling for individuals and families. Moreover, the loss of productivity due to illness and premature death contributes to economic stagnation.

The Power of Prevention

Prevention is the most effective strategy in combating the smoking epidemic. Educational campaigns highlighting the dangers of smoking, combined with regulations limiting tobacco advertising and sales, can significantly reduce smoking rates. Furthermore, support for quitting smoking, like counseling services and nicotine replacement therapies, should be readily accessible.

Personal Responsibility and Collective Action

Ultimately, the decision to stop smoking lies with the individual. However, societal support is crucial in facilitating this decision. Collective action can create an environment that discourages smoking and encourages healthier alternatives.

In conclusion, the negative implications of smoking necessitate immediate action. By understanding the risks, acknowledging the socioeconomic impact, promoting prevention, and encouraging personal responsibility, we can work towards a smoke-free future.

500 Words Essay on Stop Smoking

The health hazards of smoking.

The primary reason to quit smoking revolves around health. Cigarette smoke is a toxic mix of over 7,000 chemicals, many of which are carcinogenic. Smoking is directly linked to lung cancer, heart disease, stroke, and chronic respiratory diseases. Moreover, it weakens the immune system, making smokers more susceptible to diseases. Secondhand smoke also poses severe risks, affecting non-smokers who are exposed to it.

The Economic Impact of Smoking

Smoking also has significant economic implications. The direct cost of smoking, such as the price of cigarettes, is just the tip of the iceberg. The indirect costs, including healthcare expenses and productivity loss due to smoking-related illnesses, are substantial. In the United States alone, the total economic cost of smoking is more than $300 billion a year.

Environmental Consequences

The environmental impact of smoking is often overlooked. Cigarette butts, which are non-biodegradable, are the most littered item worldwide. They contain toxins that can leach into the environment, causing soil, water, and air pollution. The production of tobacco also contributes to deforestation and loss of biodiversity.

The Social Aspect of Smoking

Benefits of quitting smoking.

Quitting smoking brings immediate and long-term benefits. Within 20 minutes of quitting, heart rate and blood pressure drop. Within a year, the risk of heart disease is halved. Over time, the risk of stroke, lung cancer, and other diseases decrease significantly. Financially, quitting smoking can save individuals thousands of dollars annually. Environmentally, quitting reduces pollution and waste. Socially, it can improve relationships and increase social inclusion.

If you’re looking for more, here are essays on other interesting topics:

Apart from these, you can look at all the essays by clicking here .

Tobacco: Health benefits of smoking cessation

Beneficial health changes that take place:

Within 20 minutes, your heart rate and blood pressure drop.
12 hours, the carbon monoxide level in your blood drops to normal.
2-12 weeks, your circulation improves and your lung function increases.
1-9 months, coughing and shortness of breath decrease.
1 year, your risk of coronary heart disease is about half that of a smoker's.
5 years, your stroke risk is reduced to that of a nonsmoker 5 to 15 years after quitting.
10 years, your risk of lung cancer falls to about half that of a smoker and your risk of cancer of the mouth, throat, esophagus, bladder, cervix, and pancreas decreases.
15 years, the risk of coronary heart disease is that of a nonsmoker's.

Benefits in comparison with those who continued:

At about 30: gain almost 10 years of life expectancy.
At about 40: gain 9 years of life expectancy.
At about 50: gain 6 years of life expectancy.
At about 60: gain 3 years of life expectancy.
After the onset of life-threatening disease: rapid benefit, people who quit smoking after having a heart attack reduce their chances of having another heart attack by 50%.

Quitting smoking decreases the excess risk of many diseases related to second-hand smoke in children, such as respiratory diseases (e.g., asthma) and ear infections.

Quitting smoking reduces the chances of impotence, having difficulty getting pregnant, having premature births, babies with low birth weights and miscarriage.

-------------------------------------------------------------------------------------------------------------

1. Mahmud, A, Feely, J. Effect of Smoking on Arterial Stiffness and Pulse Pressure Amplification. Hypertension. 2003; 41(1):183-7.

2. U.S. Department of Health and Human Services. The Health Consequences of Smoking: Nicotine Addiction: A Report of the Surgeon General. U.S. Department of Health and Human Services, Public Health Service, Centers for Disease Control, Center for Chronic Disease Prevention and Health Promotion, Office on Smoking and Health. DHHS Publication No. (CDC) 88-8406. 1988.

3. U.S. Department of Health and Human Services. The Health Benefits of Smoking Cessation. U.S. Department of Health and Human Services, Public Health Service, Centers for Disease Control, Center for Chronic Disease Prevention and Health Promotion, Office on Smoking and Health. DHHS Publication No. (CDC) 90-8416. 1990.

4. Doll R, Peto R, Boreham J, Sutherland I. Mortality in relation to smoking: 50 years' observations on male British doctors. BMJ. 2004; 328(7455):1519-1527.

5.US Department of Health and Human Services 2004, The Health Consequences of Smoking: A Report of the Surgeon General, US Department of Health and Human Services, Centers for Disease Control and Prevention, National Center for Chronic Disease Prevention and Health Promotion, Office on Smoking and Health, 2004.

Meet Florence – the digital health worker to help you quit tobacco

World No Tobacco Day

Search the site GO Please fill out this field.
Newsletters
Health Conditions A-Z

What You Need to Know If You Want to Quit Smoking

Why It’s Hard To Quit

Complementary therapies, resisting cravings, other considerations and resources.

AndreyPopov / Getty Images

Deciding to quit smoking and taking the steps to start the cessation process can be very difficult. However, it is arguably one of the best decisions you can make for your health. In addition to causing symptoms such as a chronic cough and high blood pressure, smoking increases your risk of heart problems, cancer, respiratory diseases, and more. Smoking is the leading cause of preventable death in the United States.

Smoking cessation can cause symptoms such as a strong, overwhelming urge to smoke, irritability, and anxiety, among others. But if you’re trying to quit, help is available. Smoking cessation programs, counseling, and prescription medications can all support this process. Here’s what you need to know if you want to stop.

Benefits of Quitting Smoking

Quitting smoking improves your health, both in the long- and short-term. The benefits of cessation include:

Reduced cardiovascular risk: Quitting lowers your blood pressure and heart rate , reducing the risk of heart disease, heart attack, and other cardiovascular (heart and blood vessel) issues.
Better blood clotting: Smoking thins your blood, making it more difficult for blood to clot to stop bleeding.
Reduced cancer risk: Quitting smoking lowers your risk of developing lung cancer and other types of cancer.
Healthier lungs: Quitting allows lung tissue to heal and cilia (hair-like projections in the lungs) to regrow, which improves breathing and helps protect you from disease.
Longer lifespan: Stopping smoking raises your life expectancy by up to 10 years while also reducing your risk of premature death.
Reduced lung disease risk: Smoking can lead to emphysema and other types of chronic obstructive pulmonary disease ( COPD ); quitting prevents these and leaves you better able to fight off lung infections.
Stronger immunity: Exposing your body to the tar and nicotine from cigarettes weakens your immune system ; quitting boosts white blood cell levels, improving immunity.
Safer pregnancy: Smoking raises the chance of miscarriage and complications during pregnancy.
Increased chances of pregnancy: If you’re trying to get pregnant, quitting helps because smoking affects your estrogen levels.
Better sexual function: Quitting smoking reduces the odds you develop erectile dysfunction (an inability to achieve or maintain an erection).
Healthier bones: Smoking also impacts the health of your bones and raises your risk of fracture.
Better hearing: Smoking and breathing in someone else’s smoke (secondhand smoke) raise your risk of developing hearing loss.
Healthier eyes: Quitting tobacco can improve how well you see in the dark and lowers your risk of other vision problems.
Healthier teeth and gums: Tobacco use raises the risk of cavities, gum disease, and other dental problems.
More strength: Quitting boosts the oxygen levels in your blood, making for healthier and stronger muscles.
Clearer skin: Smoking also damages your skin ; stopping helps prevent blemishes, wrinkles, and other signs of aging.
Financial savings: Quitting can also lower your medical bills and minimize the financial impact of related illnesses; you also save money by not buying cigarettes.

There’s no denying that quitting smoking is a challenge, and you may not succeed the first time you try. That’s normal; researchers found it takes smokers in the U.S. anywhere from eight to 30 attempts before succeeding. Just remember that it’s OK if early attempts don’t work out, and don’t give up.

But what makes quitting so hard? Put simply: the nicotine in tobacco is highly addictive. If you smoke, your body acclimates to this substance, affecting everything from your metabolism and hormone levels to heart and brain function; stopping impacts you both physically and mentally.

While it only takes 24 hours without smoking for nicotine to clear from your bloodstream, withdrawal symptoms last up to one month or more. They are more severe during the first week after stopping, peaking in intensity within the first three days.

Nicotine withdrawal can cause physical, emotional , and mental health effects, including:

Tobacco cravings
Irritability
Difficulty concentrating
Increased appetite
Weight gain
Insomnia (inability to get to or stay asleep)

More severe cases of withdrawal can cause additional symptoms, such as:

Mouth ulcers
Constipation

Tobacco Triggers

Triggers add to the challenge of quitting. Triggers are situations that you associate with smoking that cause you to experience cravings. There are three types:

Social: Social triggers include being around others who are smoking, such as at a public event.
Emotional: Some people smoke to relieve stress, anxiety, boredom, or grief, making these emotional states especially triggering when you're trying not to smoke.
Pattern: Pattern or activity triggers are situations or events that you associate with smoking, like cravings in the morning, when drinking coffee, or after a meal or alcoholic drink.

What Are Smoking Cessation Programs?

Among the many tools available to help you stop are smoking cessation programs. These are individually-tailored treatment plans designed to help you quit.

There are several different types of programs: telephone-based hotlines for support, classes and coaching with trained counselors, and self-paced online courses. These approaches focus on:

Identifying your triggers and addictive patterns
Addressing the physical and emotional challenges of withdrawal
Identifying and addressing social factors surrounding smoking
Learning strategies to prevent relapse
Connecting you to support groups or other resources

What Is Smoking Cessation Counseling?

The emotional and psychological toll of quitting can be severe, lasting even after the physical effects of withdrawal have subsided. For some, individual or group sessions with a counselor trained in nicotine or drug cessation play a critical role. This typically involves regular sessions of behavioral (talk) therapy , among other techniques.

Like smoking cessation programs, counseling for nicotine use focuses on identifying strategies to keep you off tobacco products and prevent relapse. You’ll learn how to identify and cope with the patterns of your substance use as well as the mental health impact of quitting.

Products That Can Help

Currently, many products and medications can help with the physical symptoms of withdrawal. These can be divided into products that deliver nicotine to help with cravings—called nicotine replacement therapy—and prescribed medications that reduce your brain’s positive response to smoking.

Nicotine Replacement Therapy

With nicotine replacement therapy (NRT) you use products that provide nicotine to your body without the health impacts that come with smoking. Researchers have found these approaches to raise the chances of successfully quitting by 50 to 60%.

You can try NRT the moment you quit, though be sure to use the products only as indicated. There are several types:

Transdermal (worn on the skin) patches
Nasal sprays
Nasal patches

There are many NRT options, available both over the counter or with a prescription. Talk to your healthcare provider about the best choice for you.

Medications

Prescribed medications can also stop cravings and other physical symptoms. These work by blocking the nicotine from binding to receptors in your brain. This triggers the release of dopamine —the brain chemical associated with pleasure—to reduce cravings. It also reduces the dopamine released in your body if you do smoke, making it less pleasurable.

There are currently two such prescription medications on the U.S. market: Zyban (bupropion SR) and Chantix (varenicline). Dosages of these drugs are tailored to the individual, with treatment regimens lasting up to 12 weeks. Though they are generally effective, they may not be appropriate for everyone and can cause side effects like liver damage, depression, agitation, suicidal thoughts, anger, and behavioral changes.

Some people try complementary and alternative medicine methods to help with quitting, such as mindfulness training and yoga. The evidence for efficacy is often mixed and, overall, more research is needed.

Editor’s Note: This article informs you about possible observed health changes related to the use of complementary or alternative medicine based on limited available research. Not all complementary and alternative medicines have been evaluated for safety and efficacy in clinical trials. You should consult a licensed healthcare professional for diagnosis and treatment for any health conditions and inform them about any change you make to your regimen.

Mindfulness

Mindfulness encompasses talk therapies, breathing exercises, and meditation exercises . This type of therapy focuses on shifting your thoughts and feelings around your behavior and promoting relaxation to ease anxiety.

In a 2022 review studying data from 21 studies related to mindfulness and smoking cessation, the authors found no clear benefit in terms of quit rates. However, they noted that more research is needed and that mindfulness may help with the mental health impacts of quitting.

Acupuncture

Acupuncture is a complementary treatment that has origins in traditional Chinese medicine. It involves inserting fine needles into specific points in the body to stimulate nerves and other organs. For smoking, these acupuncture points are found in the ears. You can also try acupressure , which relies on physical pressure or specialized weighted balls. It’s thought these methods stimulate the nervous system and suppress cravings.

As with mindfulness, there’s a lack of conclusive evidence regarding how well acupuncture works. A review of data from 3,984 participants in 24 studies found some evidence of efficacy compared to no treatment, though little difference between acupuncture and sham treatments.

Yoga involves guided sessions of stretching, breathing, and meditation to promote relaxation and ease anxiety. Initial studies have found positive results for smoking cessation, though more research is needed.

A 2018 study of 227 smokers found that participating in regular yoga sessions increased their chances of successfully quitting. That said, there were no significant differences in quit rates when yoga was compared to general wellness classes at three and six months.

Hypnotherapy

With hypnotherapy, you work with a certified hypnotherapist to induce a heightened state of concentration and attention. It’s thought this makes you receptive to suggestions and positive changes in your life.

More research is needed to conclude whether hypnotherapy works for smoking. A 2019 review looked at 14 studies that tested hypnotherapy and smoking cessation. They found that there was little evidence to prove efficacy, and existing evidence was small at most.

The craving to smoke can not only make it difficult to avoid smoking, but it can interfere with your daily life. Thankfully, there’s actually a great deal you can do to both prevent and manage these urges.

Ways to prevent cravings include:

Spending time in public places that don’t allow smoking, such as museums, libraries, malls, or other businesses.
Avoiding drinking alcohol , coffee, or other drinks you associate with smoking.
Holding a coin, pen, or something else, especially if you miss having something in your hand.
Steering clear of the activities or people that you associate with smoking.
Exercising and ensuring you’re getting enough sleep and fluids.
Creating new habits and making sure your space is smoke-free.
Eating four to six smaller meals a day, rather than the standard two to three.
Engage in relaxing activities or meditation to cope with stress and anxiety.
Asking smokers not to smoke around you.

And if you get a craving, try the following:

Chew on cinnamon sticks, sugarless gum or lollipops, or a stick of celery.
Have healthy snacks, such as apples, carrots, or raisins.
Do some deep breathing exercises or other relaxation techniques.
Try light to moderate physical activity, such as taking a walk.
Remind yourself that the craving will pass in about 10 minutes.

You’re far from alone if you’ve tried to quit in the past and failed. According to the Centers for Disease Control and Prevention (CDC), each year, less than one in 10 Americans who try to quit succeed. It typically takes multiple tries, but every one is worth it. With support and the right resources, your odds can improve dramatically.

If you’re having trouble quitting, your healthcare provider may be able to help you assemble a smoking cessation plan. Most private insurance plans, Medicare, and Medicaid cover smoking cessation treatments. In addition, you may be able to access free support services in your city and state. Also, the National Cancer Institute has a national helpline that provides free telephone counseling.

There are many resources available for those trying to quit smoking. These include telephone counseling services (or “quitlines”), support groups, advocacy organizations, and governmental programs. You can get help from:

1-800 QUIT NOW (784-8669)
Nicotine Anonymous
Smokefree.gov
Freedom from Smoking
Tips from Former Smokers
The quitSTART app
Local or state smoking cessation programs (Google "smoking cessation programs near me")

A Quick Review

Though quitting smoking is difficult, it’s potentially the most important health decision you can make. Stopping this habit helps prevent numerous diseases and boosts your overall health, among other benefits.

Smoking cessation may involve multiple techniques, including using nicotine gum or patches, medications for cravings, as well as group or individual counseling. For most people, it takes multiple attempts to succeed; however, there are many resources available if you’re trying.

Centers for Disease Control and Prevention. Smoking and tobacco use: health effects .

American Lung Association. Tobacco facts .

National Institutes of Health. Benefits of quitting .

Centers for Disease Control and Prevention. Smoking and tobacco use: benefits of quitting .

Chang J, Ryou N, Jun HJ, Hwang SY, Song JJ, Chae SW. Effect of cigarette smoking and passive smoking on hearing impairment: data from a population–based study . PLoS ONE . 2016;11(1):e0146608. doi:10.1371/journal.pone.0146608

Chaiton M, Diemert L, Cohen JE, et al. Estimating the number of quit attempts it takes to quit smoking successfully in a longitudinal cohort of smokers . BMJ Open . 2016;6(6):e011045. doi:10.1136/bmjopen-2016-011045

National Cancer Institute. Handling nicotine withdrawal and triggers when you decide to quit tobacco .

American Academy of Family Physicians. Behavioral health and tobacco cessation .

Hartmann-Boyce J, Chepkin SC, Ye W, Bullen C, Lancaster T. Nicotine replacement therapy versus control for smoking cessation . Cochrane Database Syst Rev . 2018;5(5):CD000146. doi:10.1002/14651858.CD000146.pub5

American Cancer Society. Nicotine replacement therapy .

Jackson S, Brown J, Norris E, Livingstone-Banks J, Hayes E, Lindson N. Mindfulness for smoking cessation . Cochrane Database Syst Rev . 2022;4(4):CD013696. doi:10.1002/14651858.CD013696.pub2

Wang JH, van Haselen R, Wang M, et al. Acupuncture for smoking cessation: A systematic review and meta-analysis of 24 randomized controlled trials . Tob Induc Dis . 2019;17:48. doi:10.18332/tid/109195

Bock BC, Dunsiger SI, Rosen RK, et al. Yoga as a Complementary Therapy for Smoking Cessation: Results From BreathEasy, a Randomized Clinical Trial . Nicotine Tob Res . 2019;21(11):1517-1523. doi:10.1093/ntr/nty212

National Center for Complementary and Alternative Medicine. Complementary health approaches for smoking cessation: what the science says .

Barnes J, McRobbie H, Dong CY, Walker N, Hartmann-Boyce J. Hypnotherapy for smoking cessation . Cochrane Database Syst Rev . 2019;6(6):CD001008. doi:10.1002/14651858.CD001008.pub3

Centers for Disease Control and Prevention. Smoking cessation: fast facts .

Our Writers
How to Order
Assignment Writing Service
Report Writing Service
Buy Coursework
Dissertation Writing Service
Research Paper Writing Service
All Essay Services
Buy Research Paper
Buy Term Paper
Buy Dissertation
Buy Case study
Buy Presentation
Buy Personal statement

Persuasive Essay Guide

Persuasive Essay About Smoking

Persuasive Essay About Smoking - Making a Powerful Argument with Examples

What You Need To Know About Persuasive Essay

A persuasive essay is a type of writing that aims to convince its readers to take a certain stance or action. It often uses logical arguments and evidence to back up its argument in order to persuade readers.

It also utilizes rhetorical techniques such as ethos, pathos, and logos to make the argument more convincing. In other words, persuasive essays use facts and evidence as well as emotion to make their points.

A persuasive essay about smoking would use these techniques to convince its readers about any point about smoking. Check out an example below:

Simple persuasive essay about smoking

Tough Essay Due? Hire Tough Writers!

Persuasive Essay Examples About Smoking

Smoking is one of the leading causes of preventable death in the world. It leads to adverse health effects, including lung cancer, heart disease, and damage to the respiratory tract. However, the number of people who smoke cigarettes has been on the rise globally.

A lot has been written on topics related to the effects of smoking. Reading essays about it can help you get an idea of what makes a good persuasive essay.

Here are some sample persuasive essays about smoking that you can use as inspiration for your own writing:

Persuasive speech on smoking outline

Persuasive essay about smoking should be banned

Persuasive essay about smoking pdf

Persuasive essay about smoking cannot relieve stress

Persuasive essay about smoking in public places

Speech about smoking is dangerous

Persuasive Essay About Smoking Introduction

Persuasive Essay About Stop Smoking

Short Persuasive Essay About Smoking

Stop Smoking Persuasive Speech

Check out some more persuasive essay examples on various other topics.

Argumentative Essay About Smoking Examples

An argumentative essay is a type of essay that uses facts and logical arguments to back up a point. It is similar to a persuasive essay but differs in that it utilizes more evidence than emotion.

If you’re looking to write an argumentative essay about smoking, here are some examples to get you started on the arguments of why you should not smoke.

Argumentative essay about smoking pdf

Argumentative essay about smoking in public places

Argumentative essay about smoking introduction

Check out the video below to find useful arguments against smoking:

Tips for Writing a Persuasive Essay About Smoking

You have read some examples of persuasive and argumentative essays about smoking. Now here are some tips that will help you craft a powerful essay on this topic.

Choose a Specific Angle

Select a particular perspective on the issue that you can use to form your argument. When talking about smoking, you can focus on any aspect such as the health risks, economic costs, or environmental impact.

Think about how you want to approach the topic. For instance, you could write about why smoking should be banned.

Check out the list of persuasive essay topics to help you while you are thinking of an angle to choose!

Research the Facts

Before writing your essay, make sure to research the facts about smoking. This will give you reliable information to use in your arguments and evidence for why people should avoid smoking.

You can find and use credible data and information from reputable sources such as government websites, health organizations, and scientific studies.

For instance, you should gather facts about health issues and negative effects of tobacco if arguing against smoking. Moreover, you should use and cite sources carefully.

Paper Due? Why Suffer? That's our Job!

Make an Outline

The next step is to create an outline for your essay. This will help you organize your thoughts and make sure that all the points in your essay flow together logically.

Your outline should include the introduction, body paragraphs, and conclusion. This will help ensure that your essay has a clear structure and argument.

Use Persuasive Language

When writing your essay, make sure to use persuasive language such as “it is necessary” or “people must be aware”. This will help you convey your message more effectively and emphasize the importance of your point.

Also, don’t forget to use rhetorical devices such as ethos, pathos, and logos to make your arguments more convincing. That is, you should incorporate emotion, personal experience, and logic into your arguments.

Introduce Opposing Arguments

Another important tip when writing a persuasive essay on smoking is to introduce opposing arguments. It will show that you are aware of the counterarguments and can provide evidence to refute them. This will help you strengthen your argument.

By doing this, your essay will come off as more balanced and objective, making it more convincing.

Finish Strong

Finally, make sure to finish your essay with a powerful conclusion. This will help you leave a lasting impression on your readers and reinforce the main points of your argument. You can end by summarizing the key points or giving some advice to the reader.

A powerful conclusion could either include food for thought or a call to action. So be sure to use persuasive language and make your conclusion strong.

To conclude,

By following these tips, you can write an effective and persuasive essay on smoking. Remember to research the facts, make an outline, and use persuasive language.

However, don't stress if you need expert help to write your essay! Our professional essay writing service is here for you!

Our persuasive essay writing service is fast, affordable, and trustworthy.

Try it out today!

Write Essay Within 60 Seconds!

Caleb S. has been providing writing services for over five years and has a Masters degree from Oxford University. He is an expert in his craft and takes great pride in helping students achieve their academic goals. Caleb is a dedicated professional who always puts his clients first.

Paper Due? Why Suffer? That’s our Job!

Keep reading

Official websites use .gov

A .gov website belongs to an official government organization in the United States.

Secure .gov websites use HTTPS

A lock ( ) or https:// means you've safely connected to the .gov website. Share sensitive information only on official, secure websites.

7 Common Withdrawal Symptoms

And What You Can Do About Them

Trying to quit smoking feels different for each person, but almost everyone will have some symptoms of nicotine withdrawal. When you stop, your body and brain have to get used to not having nicotine. This can be uncomfortable, but nicotine withdrawal can’t hurt you – unless you give in and have a cigarette!

Over time, withdrawal symptoms will fade as long as you stay smokefree.

1. Having urges or cravings to smoke

Direction street sign with Help, Support, Advice, Guidance, Assistance and Info.

Almost everyone who smokes regularly has cravings or urges to smoke when they quit. They may be mild or can sometimes feel overwhelming. Figuring out how to deal with cravings is one of the most important things you can do to stay successful.

Ways to manage: There are LOTS of things you can do to make urges and cravings less of a problem. Quit-smoking medicines can help a lot, and so can other quitting tips . Cravings can be triggered by things that make you think about smoking—like people you smoked with, a place you often smoked, or things you used to do while smoking like having a cup of coffee. Even a thought or a feeling can trigger a craving. But other thoughts can help you get through a craving, like remembering why you are quitting. Remember that you never have to give in to a craving, and that it will always pass.

Use a quit-smoking medicine.
Keep busy and distract yourself.
Be active – some physical activity is better than none!
Spend time with friends who don’t smoke.
See other ways to manage withdrawal .

2. Feeling irritated, grouchy, or upset

It is very common to feel irritated or grouchy when you quit. Even many people who have never smoked know this is part of quitting. Knowing this is normal can be helpful.

Ways to manage: Remind yourself that you likely feel this way because your body is getting used to being without nicotine. Take a few deep breaths and remind yourself why you’re quitting.

3. Feeling jumpy and restless

Feeling jumpy or restless during the first days or weeks after quitting is normal. Just like your mind gets irritated without nicotine at first, the rest of your body can, too.

Ways to manage: Doing some physical activity can help shake loose your jumpiness. Get up and walk around for a bit if you feel restless. Try cutting back on coffee, tea, and other caffeinated drinks. When you quit smoking, caffeine lasts longer in your body.

4. Having a hard time concentrating

You may notice that it is harder to concentrate in the first days after you quit—this is very common.

Ways to manage: Try to cut yourself some slack, especially in the first days after you quit. Try to limit activities that require strong concentration if you can.

5. Having trouble sleeping

It’s common to have some trouble sleeping when you first quit smoking. This will get better, but if it is bothering you, talk with your healthcare provider to get help. If you become exhausted from poor sleep, this can make it harder to stay quit.

Ways to manage:

If you drink coffee, tea, or other caffeinated drinks regularly, don’t drink them in the late afternoon or evening. When you quit smoking, caffeine lasts longer in your body.
If you are using the nicotine patch, try taking it off an hour before bedtime. Sometimes the nicotine in the patch can affect your sleep.
Don’t watch TV or use phones, computers, or e-books in bed.
Make sure your bedroom is quiet, dark, relaxing, and at a comfortable temperature.
Don’t eat a heavy meal or drink alcohol right before bed.
Add in some physical activity during the day (but not right before bed).
Go to sleep and wake up around the same time each day, even on weekends.

6. Feeling hungrier or gaining weight

It’s normal for your appetite to increase some when you quit. And your body may not burn calories quite as fast. You may also eat more because of the stress of quitting or to have something to do with your hands and mouth. Food may even be more enjoyable because your senses of smell and taste are not being dulled by all that smoke!

Ways to manage: While some people may gain weight after they quit, it’s important for your health to quit sooner than later. Below are a few simple things you can do to help control weight gain after quitting. The bonus is that these things will help you build healthy behaviors for a lifetime of being smokefree!

Snack smart. If you eat between meals, find some healthy, low-calorie foods that still give your mouth and hands something to do, like celery, carrots, or sugar-free mints. You can also keep your hands and mouth busy with a toothpick or a straw.
Be active. Any physical activity is better than none. Even if you don’t want to join a gym or take up running, simply going for a walk can have real health benefits!
When you eat, focus on eating. Eating is often something we do in the background while we watch TV or check our phones. When we eat like this, we eat more. When you quit smoking, make a point of removing distractions when you eat. Also try eating a bit slower and focus on enjoying your food. This can help you notice when you are getting full.

If you are worried about gaining weight , a quit coach can help you with other quitting tips , or you can talk with your healthcare provider for help.

7. Feeling anxious, sad, or depressed

People who smoke are more likely to have anxiety or depression than people who don’t smoke. Some people feel mood changes for a short time after they quit smoking. Watch for this, especially if you’ve ever had anxiety or depression.

For some people, smoking may seem like it helps with anxiety or depression, but don’t be tricked. Smoking might make you feel better in the short-term, but that’s because the nicotine in cigarettes stops the discomfort of withdrawal, not because it is helping with anxiety or depression. There are much better ways to deal with withdrawal symptoms and mood changes than returning to smoking! The good news is that once people have been smoke-free for a few months, their anxiety and depression levels are often lower than when they were smoking.

Be Active. Being physically active can help lift your mood. Start small and build up over time. This can be hard to do if you’re feeling down. But your efforts will pay off.
Structure your day. Stay busy. Get out of the house if you can.
Connect with other people. Being in touch or talking with others every day can help your mood. Try to connect with people who are supportive of your efforts to quit smoking.
Reward yourself. Do things you enjoy. Even small things add up and help you feel better.
Talk with a healthcare provider. If you don’t feel better in a couple weeks, or your symptoms feel unmanageable, it’s important to contact a healthcare provider.

What if feelings of depression get worse, or don’t get better? You should get help . Talk to your healthcare provider, call the quitline ( 1-800-QUIT-NOW ), or seek appropriate emergency help.

Call or text the 988 Suicide & Crisis Lifeline at 988 , available 24 hours a day, 7 days a week. Online chat external icon is available 24/7.
Call 911 or go to the nearest hospital emergency department for emergency medical treatment.
Don’t be alone. Don’t leave another person alone if he or she is in crisis.

To receive email updates about this page, enter your email address:

Smoking & Tobacco Use
Smokefree.gov
National Cancer Institute

Exit Notification / Disclaimer Policy

The Centers for Disease Control and Prevention (CDC) cannot attest to the accuracy of a non-federal website.
Linking to a non-federal website does not constitute an endorsement by CDC or any of its employees of the sponsors or the information and products presented on the website.
You will be subject to the destination website's privacy policy when you follow the link.
CDC is not responsible for Section 508 compliance (accessibility) on other federal or private website.

Alzheimer's disease & dementia
Arthritis & Rheumatism
Attention deficit disorders
Autism spectrum disorders
Biomedical technology
Diseases, Conditions, Syndromes
Endocrinology & Metabolism
Gastroenterology
Gerontology & Geriatrics
Health informatics
Inflammatory disorders
Medical economics
Medical research
Medications
Neuroscience
Obstetrics & gynaecology
Oncology & Cancer
Ophthalmology
Overweight & Obesity
Parkinson's & Movement disorders
Psychology & Psychiatry
Radiology & Imaging
Sleep disorders
Sports medicine & Kinesiology
Vaccination
Breast cancer
Cardiovascular disease
Chronic obstructive pulmonary disease
Colon cancer
Coronary artery disease
Heart attack
Heart disease
High blood pressure
Kidney disease
Lung cancer
Multiple sclerosis
Myocardial infarction
Ovarian cancer
Post traumatic stress disorder
Rheumatoid arthritis
Schizophrenia
Skin cancer
Type 2 diabetes
Full List »

share this!

June 4, 2024

This article has been reviewed according to Science X's editorial process and policies . Editors have highlighted the following attributes while ensuring the content's credibility:

fact-checked

trusted source

Study finds methods to quit smoking effective regardless of mental health history

by Public Library of Science

Sarah Jackson and colleagues from University College London and King's College London branches of the SPECTRUM Consortium conducted a survey to study how mental health relates to methods people use to quit smoking, also known as smoking cessation aids.

While the number of adults who smoke cigarettes has declined globally, people with mental health conditions are more likely to smoke and to do so more heavily. Because of these differences in tobacco use , the researchers theorized that the effectiveness of smoking cessation aids may be altered in individuals with a mental health condition.

However, in their findings published in PLOS Mental Health , they report that smoking cessation aids are actually equally effective for people with and without a history of mental health conditions.

The researchers surveyed over 5,000 people who regularly smoked and attempted to quit in the past year. About 45% of these participants reported having been diagnosed with a mental health condition. In line with previous studies, participants with mental health conditions reported a higher level of addiction to cigarettes.

The methods participants used in their attempts to quit smoking ranged widely. The most common smoking cessation aids were non-combustible nicotine products. Vaping products ( e-cigarettes ) were used by 39% of people with a mental health condition and 31% of people without.

The next most common aids were other over-the-counter nicotine replacements, such as lozenges and patches. Less than 5% of participants reported using other aids like prescription medications or behavioral interventions.

People with mental health conditions were more likely than those without to choose vaping products, prescription nicotine replacement therapy, and self-help websites. However, the researchers found that a person's mental health condition did not appear to alter the effectiveness of these smoking cessation aids or any others.

Among all participants, the researchers report that the most effective aids were vaping, a drug called varenicline that interacts with nicotine receptors in the brain, and heated tobacco products. Heated tobacco products are a new type of smoking cessation aid that heats tobacco leaves but does not burn them, and this study is the first to look at their real-world effectiveness. The researchers did not find clear benefits of using any of the other smoking cessation aids.

The results of this study can help smokers and health care workers make informed decisions when choosing methods to quit smoking. The researchers note that, "We found no evidence to suggest that any method of stopping smoking was more or less effective for people with a history of mental health conditions. Our findings should provide reassurance to people with mental health conditions who want to stop smoking that their condition need not affect their choice of cessation aid."

Explore further

Feedback to editors

Novel analysis methods used for Huntington's disease

10 hours ago

Glowing dye may help surgeons eradicate prostate cancer

Research identifies issues with booking new appointments at clinics for cancer treatment

Jun 8, 2024

What makes roads safer? New study uses AI to find out

Socially connected older adults hit harder by pandemic than isolated peers

Girl in Australia, 2, struck with H5N1 bird flu: WHO

Clinical trial shows 15-day Paxlovid regimen safe but adds no clear benefit for long COVID

Jun 7, 2024

Unlocking another piece of the Parkinson's puzzle—scientists reveal workings of vital molecular switch

Antioxidant gel preserves islet function after pancreas removal: New approach could reduce diabetes complications

More evidence suggests regular consumption of melatonin can reduce chances of age-related macular degeneration

E-cigarettes boost tobacco use abstinence with smoking cessation counseling

Feb 19, 2024

New study shows quitting smoking can improve mental health

Jun 1, 2023

Should e-cigarettes be licensed as medicines?

Jan 12, 2022

E-cigarettes help pregnant smokers quit without risks to pregnancy, trial finds

Jan 17, 2024

Only 1 in 4 rural US smokers attempted to quit during a one year period, study finds

Mar 5, 2024

E-cigarettes found to help more tobacco smokers quit than traditional nicotine replacement

Jan 8, 2024

Recommended for you

Bartonella DNA found in blood of patients with psychosis

Researchers say that people experiencing homelessness and addiction should not be excluded from exercise interventions

The body's own lipids affect mental disorders: Can specific inhibitors help?

Jun 6, 2024

New study challenges 'pop psychology' myths about habits

Younger children are more commonly diagnosed with ADHD than their older classmates, says new study

Digital games may be an overlooked ally in mental health

Let us know if there is a problem with our content.

Use this form if you have come across a typo, inaccuracy or would like to send an edit request for the content on this page. For general inquiries, please use our contact form . For general feedback, use the public comments section below (please adhere to guidelines ).

Please select the most appropriate category to facilitate processing of your request

Thank you for taking time to provide your feedback to the editors.

Your feedback is important to us. However, we do not guarantee individual replies due to the high volume of messages.

E-mail the story

Your email address is used only to let the recipient know who sent the email. Neither your address nor the recipient's address will be used for any other purpose. The information you enter will appear in your e-mail message and is not retained by Medical Xpress in any form.

Newsletter sign up

Get weekly and/or daily updates delivered to your inbox. You can unsubscribe at any time and we'll never share your details to third parties.

More information Privacy policy

Donate and enjoy an ad-free experience

We keep our content available to everyone. Consider supporting Science X's mission by getting a premium account.

E-mail newsletter

Loading metrics

Open Access

Peer-reviewed

Research Article

Moderation of the real-world effectiveness of smoking cessation aids by mental health conditions: A population study

Roles Conceptualization, Formal analysis, Investigation, Methodology, Writing – original draft

* E-mail: [email protected]

Affiliations Department of Behavioural Science and Health, University College London, London, United Kingdom, SPECTRUM Consortium, London, United Kingdom

Roles Conceptualization, Funding acquisition, Investigation, Methodology, Writing – review & editing

Affiliations SPECTRUM Consortium, London, United Kingdom, Addictions Department, Institute of Psychiatry, Psychology and Neuroscience, King’s College London, London, United Kingdom

Roles Conceptualization, Data curation, Investigation, Methodology, Writing – review & editing

Roles Conceptualization, Investigation, Methodology, Writing – review & editing

Roles Conceptualization, Data curation, Funding acquisition, Investigation, Methodology, Supervision, Writing – review & editing

Sarah E. Jackson,
Leonie Brose,
Vera Buss,
Lion Shahab,
Deborah Robson,
Jamie Brown

Published: June 4, 2024
https://doi.org/10.1371/journal.pmen.0000007
Peer Review
Reader Comments

To examine whether the real-world effectiveness of popular smoking cessation aids differs between users with and without a history of mental health conditions.

Nationally-representative cross-sectional survey conducted monthly between 2016–17 and 2020–23.

Participants

5,593 adults (2,524 with a history of ≥1 mental health conditions and 3,069 without) who had smoked regularly within the past year and had attempted to quit at least once in the past year.

Main outcome measures

The outcome was self-reported abstinence from quit date up to the survey. Independent variables were use of the following cessation aids during the most recent quit attempt: prescription nicotine replacement therapy (NRT), NRT over-the-counter, varenicline, bupropion, vaping products, face-to-face behavioural support, telephone support, written self-help materials, websites, hypnotherapy, Allen Carr’s Easyway, heated tobacco products, and nicotine pouches. The moderator was history of diagnosed mental health conditions (yes/no). Covariates included sociodemographic characteristics, level of cigarette addiction, and characteristics of the quit attempt.

Relative to those without, participants with a history of mental health conditions were significantly more likely to report using vaping products (38.8% [95%CI 36.7–40.8] vs. 30.7% [28.9–32.5]), prescription NRT (4.8% [3.9–5.7] vs. 2.7% [2.1–3.3]), and websites (4.0% [3.2–4.8] vs. 2.2% [1.6–2.7]). Groups did not differ significantly in their use of other aids. After adjusting for covariates and use of other cessation aids, those who used vaping products (OR = 1.92, 95%CI 1.61–2.30), varenicline (OR = 1.88, 95%CI 1.19–2.98), or heated tobacco products (OR = 2.33, 95%CI 1.01–5.35) had significantly higher odds of quitting successfully than those who did not report using these aids. There was little evidence that using other cessation aids increased the odds of successful cessation, or that the user’s history of mental health conditions moderated the effectiveness of any aid.

Conclusions

Use of vaping products, varenicline, or heated tobacco products in a quit attempt was associated with significantly greater odds of successful cessation, after adjustment for use of other cessation aids and potential confounders. There was no evidence to suggest the effectiveness of any popular cessation aid differed according to the user’s history of mental health conditions.

Citation: Jackson SE, Brose L, Buss V, Shahab L, Robson D, Brown J (2024) Moderation of the real-world effectiveness of smoking cessation aids by mental health conditions: A population study. PLOS Ment Health 1(1): e0000007. https://doi.org/10.1371/journal.pmen.0000007

Editor: Sasidhar Gunturu, BronxCare Health System, UNITED STATES

Received: December 4, 2023; Accepted: March 6, 2024; Published: June 4, 2024

Copyright: © 2024 Jackson et al. This is an open access article distributed under the terms of the Creative Commons Attribution License , which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

Data Availability: Data used in these analyses are available on Open Science Framework ( https://osf.io/5xubc/ ).

Funding: This work was supported by CRUK (PRCRPG-Nov21\100002 to JB) and UK Prevention Research Partnership (MR/S037519/1 to LB). The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.

Competing interests: We have read the journal’s policy and the authors of this manuscript have the following competing interests: JB has received unrestricted research funding from Pfizer and J&J, who manufacture smoking cessation medications. LS has received honoraria for talks, an unrestricted research grant and travel expenses to attend meetings and workshops from Pfizer, and has acted as paid reviewer for grant awarding bodies and as a paid consultant for health care companies. All authors declare no financial links with tobacco companies, e-cigarette manufacturers, or their representatives. There are no patents, products in development or marketed products associated with this research to declare. This does not alter our adherence to PLOS ONE policies on sharing data and materials.

Introduction

Tobacco smoking remains a leading cause of preventable illness and premature mortality in England [ 1 ]. Relative to the general population, people with mental health conditions are more likely to smoke, smoke more heavily, and show greater signs of dependence [ 2 – 5 ]. They are also at increased risk of tobacco-related morbidities, including cardiovascular disease [ 6 , 7 ], which causes them to have substantially lower life expectancy [ 8 , 9 ]. Quitting smoking can reduce these risks [ 10 ]. A range of smoking cessation aids have been found to increase successful smoking cessation in randomised controlled trials (RCTs) [ 11 – 14 ] and in real-world settings [ 15 – 24 ]. Understanding whether and, if so, how far their effectiveness differs between people with and without mental health conditions can help health professionals and patients to make informed choices around the use of aids for smoking cessation.

In England, a comprehensive range of smoking cessation medications and behavioural support are available [ 25 ]. Pharmacological aids include nicotine replacement therapy (NRT), which is available free of charge on prescription or can be bought over-the-counter (OTC), and varenicline (Champix) and bupropion (Zyban) which are only available on prescription. The supply of Champix, the most effective of these [ 14 , 23 , 24 ], was disrupted in 2021 due to nitrosamine impurities found by its supplier, Pfizer [ 26 ]. The supply of Zyban was disrupted in late 2022 due to similar concerns about nitrosamine impurities found by its supplier, GSK [ 27 ]. Both medications remain unavailable as of March 2024. Generic versions of varenicline are available in other countries and cytisine, a drug with similar properties to varenicline, is licensed [ 28 ] and has begun to be supplied in England since January 2024.

Vaping products (often referred to as e-cigarettes) and nicotine pouches are available from specialist ‘vape shops’, supermarkets, smaller convenience stores, and online [ 29 ]. Heated tobacco products have been available in the UK since 2016 but their efficacy for smoking cessation is uncertain [ 30 ]. Smokers also have access to free dedicated stop smoking services, which offer behavioural support, pharmacotherapy, and in some cases, vaping products [ 31 ]. Telephone support is available via a free Smokefree National Helpline, and websites offer information on quitting, other forms of support available, and how to access them. Other behavioural treatments, including hypnotherapy and Allen Carr’s Easyway method (a single-session pharmacotherapy-free behavioural programme) [ 32 , 33 ], are provided by private companies.

Around one in two attempts to stop smoking in England involves the use of at least one of these cessation aids [ 34 ]. Vaping products are most commonly used (~30% of quit attempts), followed by NRT available OTC (~10%) and medications obtained on prescription (NRT, varenicline, or bupropion; ~5%) [ 34 ].

It is possible that the effectiveness of these smoking cessation aids may differ between people with and without mental health conditions [ 35 ]. People with mental health conditions may experience stronger reinforcing effects of nicotine, more severe withdrawal symptoms when they try to quit, and greater cessation fatigue (being tired of trying to stop smoking) [ 36 ]. As such, it is possible that they may benefit more from cessation aids that mimic the effect of nicotine (e.g., varenicline) or provide an alternative source of nicotine (e.g., NRT, vaping products, nicotine pouches) and less from other cessation aids (e.g., forms of behavioural support). On the other hand, people with mental health conditions may be less likely to adhere to treatments [ 37 ], causing effectiveness to be lower.

To our knowledge, just two large experimental studies have investigated whether the effectiveness of smoking cessation treatments is moderated by a person’s mental health status. These have focused on varenicline, bupropion, and NRT. One large RCT (‘EAGLES’) compared varenicline and bupropion with nicotine patch and placebo and showed similar efficacy of these medications for smokers with and without psychiatric disorders [ 38 ]. However, a recent secondary analysis of another RCT that compared the effectiveness of bupropion and varenicline reported a slightly different pattern of results [ 39 ]. While varenicline was associated with similar quitting outcomes for smokers with depressive symptoms than those without, bupropion appeared to be less effective as a smoking cessation aid for those with depressive symptoms [ 39 ]. Further research is required on these and other cessation aids. Observational data can shed light on any differences in treatment effectiveness in real-world settings [ 40 ].

Using data from the Smoking Toolkit Study, a large, nationally-representative survey of adults in England, this study aimed to comprehensively examine whether the real-world effectiveness of popular smoking cessation aids differs between users with and without mental health conditions. Data on smoking status in relation to history of mental health conditions have been published elsewhere [ 2 ], so this paper focused specifically on the use and effectiveness of different cessation aids among those attempting to quit smoking. Specifically, we aimed to address the following research questions:

To what extent does a history of one or more diagnosed mental health conditions moderate associations between use (vs. non-use) of various cessation aids in a quit attempt and chances of success?
Are any moderating effects similar for those with a single mental health condition and those with multiple mental health conditions?

Materials and methods

Pre-registration.

The study protocol and analysis plan were pre-registered on Open Science Framework (osf.io/5xubc). We made one amendment. We had planned to calculate Bayes factors for non-significant interactions based on an expected effect size of OR = 1.5 in the observed direction (i.e., OR = 1.5 for observed ORs >1 and OR = 0.67 for observed ORs <1). Instead, we calculated Bayes factors in both directions, to offer more insight into whether the data suggested a given aid was more or less effective for people with a history of mental health conditions than those without.

This was an observational study using data from the Smoking Toolkit Study; a nationally-representative monthly cross-sectional survey of adults (≥16 years) in England [ 41 ]. The study uses a hybrid of random probability and simple quota sampling to select a new sample of approximately 1,700 adults aged ≥16 years each month. Comparisons with other national surveys and sales data indicate that the survey obtains nationally-representative estimates for key variables including sociodemographic characteristics, smoking prevalence, and cigarette consumption [ 41 , 42 ]. The Smoking Toolkit Study is coordinated by this study’s authors at University College London (PI Jamie Brown).

Data collection for the Smoking Toolkit Study began in November 2006 and the study continues to collect data from a new sample each month. Up to February 2020, the survey was conducted via face-to-face computer-assisted interviews. However, social distancing restrictions introduced during the Covid-19 pandemic meant that no data were collected in March 2020, and data from April 2020 onwards have been collected via telephone interviews. The telephone interviews use a similar sampling and weighting approach as the face-to-face interviews and data collected via the two modalities show good comparability [ 43 – 45 ]. Data were not collected from 16 and 17 year olds between April 2020 and December 2021.

While a core set of questions is included in each monthly survey, other variables are only assessed in certain waves, depending on availability of competitive research funding. Questions on mental health have been collected in two periods: January 2016-December 2017 and October 2020-June 2023. We used data from participants surveyed in these periods. We selected participants aged ≥18 years who:

smoked cigarettes (including hand-rolled) or any other tobacco product (e.g., pipe or cigar) daily or occasionally at the time of the survey or during the past year; and
reported having made at least one serious quit attempt in the past year.

Ethics statement

Ethical approval was provided by the UCL Research Ethics Committee (0498/001). Participants provided informed verbal consent to take part in the study, and all methods are carried out in accordance with relevant regulations. The data are not collected by UCL and are anonymised when received by UCL.

Outcome: Successful smoking cessation.

The outcome variable was self-reported continuous abstinence from the start of the most recent quit attempt up to the time of survey. Respondents were asked ‘How long did your most recent quit attempt last before you went back to smoking?’ Responses were coded 1 for those who responded that they were still not smoking and 0 otherwise.

Exposures: Use of cessation aids.

Independent variables were self-reported use or not (dummy coded) of the following smoking cessation aids in the most recent quit attempt: prescription NRT (available in England from prescribing health professionals, including advisors at specialist stop smoking services); NRT available OTC; varenicline; bupropion; vaping products; face-to-face behavioural support; telephone support; written self-help materials; websites; hypnotherapy; Allen Carr’s Easyway; heated tobacco products; and nicotine pouches.

Respondents were asked to indicate all that apply, and data for each were coded 1 if chosen and 0 if not. Heated tobacco products were included in the list of response options from April 2016 and nicotine pouches from June 2021; given the low prevalence of use of these products [ 46 , 47 ], we imputed missing values as 0 for participants surveyed before the response options were introduced.

Moderator: History of mental health conditions.

Diagnosed mental health conditions were assessed with the question: ‘Since the age of 16, which of the following, if any, has a doctor or health professional ever told you that you had?’ followed by a list of ICD-10 recognised conditions: depression; anxiety; obsessive compulsive disorder; panic disorder or a phobia; post-traumatic stress disorder; psychosis; personality disorder; attention deficit hyperactivity disorder; an eating disorder; alcohol misuse or dependence; drug use or dependence; and problem gambling. Between 2020 and 2023, this list also included: autism or autism spectrum disorder; and bipolar disorder.

For our primary analysis (RQ1), those who reported any of these diagnoses were coded 1, else they were coded 0 (including those who did not respond, responded ‘don’t know’, or ‘prefer not to say’).

For our secondary analysis (RQ2), we subdivided the group reporting mental health diagnoses to create a three-level variable: no history of mental health conditions (coded 0), single mental health condition (1 diagnosis; coded 1), and multiple mental health conditions (≥2 diagnoses; coded 2), given previous evidence showing stronger associations with smoking outcomes among those with multiple conditions [ 2 ].

Covariates.

Covariates included a range of sociodemographic characteristics, level of cigarette addiction, and variables relating to the most recent quit attempt.

Sociodemographic covariates included age, gender, and occupational social grade (ABC1, which includes managerial, professional and intermediate occupations, vs. C2DE, which includes lower supervisory and technical occupations, semi‐routine and routine occupations, never worked and long‐term unemployed).

Level of cigarette addiction was assessed by asking participants to self-report ratings of the strength of urges to smoke over the last 24 hours (not at all (coded 0), slight (1), moderate (2), strong (3), very strong (4), extremely strong (5)). This question was also coded ‘0’ for smokers who respond ‘not at all’ to the (separate) question ‘How much of the time have you spent with the urge to smoke?’ [ 48 ]. This validated measure has similar predictive value as the Fagerström Test of Cigarette Dependence and the Heaviness of Smoking Index in for cessation [ 49 ].

The characteristics of the most recent quit attempt included time since the quit attempt started (<1 month, 1–6 months, >6 months), the number of prior quit attempts in the past year (1, 2, 3 or ≥4), whether the quit attempt was planned, and whether the respondent cut down first or stopped abruptly.

The month and year of survey were also included to account for seasonal variation in quit attempts (e.g., in January or ‘Stoptober’ [ 50 , 51 ]) and changes in the availability and regulation of different smoking cessation aids over the study period. We also adjusted for the mode of data collection with a variable coded 0 up to February 2020 (when data were collected face to face) and 1 from April 2020 onwards (when data were collected via telephone).

Statistical analysis

The Smoking Toolkit Study uses survey weights to adjust data so that the sample matches the demographic profile of England on age, social grade, region, housing tenure, ethnicity and working status within sex [ 41 ]. The following analyses used weighted data. Missing values were excluded on a per-analysis basis.

We calculated the proportion and 95% confidence interval (CI) of smokers with and without mental health conditions reporting using each cessation aid in the most recent quit attempt, and the quit success rate among users of each aid. We also provided descriptive data on the proportion reporting using each cessation aid and the overall quit success rate separately for each individual mental health condition.

We used logistic regression to analyse associations between self-reported abstinence (abstinent yes vs. no) and use of different smoking cessation aids (use of a specific aid vs. no use of that specific aid), adjusting for mental health status, covariates, and use of other cessation aids (baseline model). We repeated the baseline model with the addition of the two-way interaction between mental health diagnoses (0 vs ≥1 mental health conditions) and each cessation aid in turn.

To explore any differences between those with single and multiple mental health diagnoses, we reran the interactions using a 3-level mental health variable (0, 1, ≥2 mental health conditions).

We calculated Bayes factors using an online calculator (bayesfactor.info) to aid in the interpretation of non-significant interactions with mental health diagnoses. These enabled us to examine whether these associations could best be characterised as evidence of no effect, evidence of an effect, or whether data were insensitive to detect an effect [ 52 , 53 ]. Alternative hypotheses were represented by half-normal distributions and the expected effect size set to OR = 1.5 in the observed direction (OR = 1.5 where the observed OR was >1 and OR = 0.67 when the observed OR was <1) [ 23 ].

Of 95,952 participants surveyed in eligible waves, 17,394 (18.1%) reported smoking in the past year, of whom 5,741 (33.0%) attempted to stop smoking in the past year. We excluded 148 participants with missing data on mental health conditions (there were no missing data on use of cessation aids), leaving a final sample for analysis of 5,593 participants.

Just under half (45.1% weighted) of participants reported having ever been diagnosed with a mental health condition; 16.8% reported a single mental health condition and 28.3% multiple conditions. Table 1 summarises the characteristics of participants with and without a history of mental health conditions. S1 Table presents corresponding data for those reporting single and multiple mental health conditions. Relative to those without, participants reporting a history of mental health conditions were more likely to be younger, identify as women or non-binary, and come from less advantaged social grades. They also reported a higher level of cigarette addiction, on average, but there were no notable differences in the characteristics of their most recent quit attempt.

PPT PowerPoint slide
PNG larger image
TIFF original image

https://doi.org/10.1371/journal.pmen.0000007.t001

Table 2 summarises use of cessation aids by participants’ history of mental health conditions. Participants with a history of mental health conditions were significantly more likely to report using one or more cessation aids (58.9%) than those without (52.9%) and to report using multiple aids (12.0% vs. 7.3%). Among those with and without a history of mental health conditions, vaping products were the most commonly used aid (38.8% and 30.7%, respectively), followed by NRT available over-the-counter (16.7% and 17.8%). All other aids were used by <5% of participants. Relative to those without, participants with a history of mental health conditions were more likely to report using vaping products, prescription NRT, and websites. Use of other aids did not differ significantly between groups. There was no significant difference in the prevalence of use of any cessation aid between those with single versus multiple mental health conditions ( S2 Table ).

https://doi.org/10.1371/journal.pmen.0000007.t002

Table 2 also shows unadjusted quit success rates for those using each cessation aid. Although absolute differences appeared large for some aids (e.g., written self-help materials and nicotine pouches), wide confidence intervals meant there was no statistically significant difference in quit rates between users of aids with and without a history of mental health conditions, before adjustment for potential confounding variables and use of other aids.

Table 3 shows the results of the logistic regression analyses. The baseline model, which included use (vs. non-use) of each cessation aid, history of mental health conditions, and covariates, indicated participants who used vaping products (OR = 1.92, 95%CI 1.61–2.30), varenicline (OR = 1.88, 95%CI 1.19–2.98), or heated tobacco products (OR = 2.33, 95%CI 1.01–5.35) in their quit attempt had significantly higher odds of quitting successfully than those who did not. Those who used Allen Carr’s Easyway method (either via face-to-face session [19.8%], book [66.9%], or both [13.3%]) had significantly lower odds of quitting successfully than those who did not (OR = 0.41, 95%CI 0.18–0.94). Use of other aids was not significantly associated with odds of quit success, after adjustment.

https://doi.org/10.1371/journal.pmen.0000007.t003

Tests of interactions showed no statistically significant moderating effect of history of mental health conditions on the effectiveness of any cessation aid ( Table 3 ). Bayes factors indicated the data were largely insensitive to distinguish between evidence of moderation and no evidence of moderation, meaning we were unable to rule out potential differences in effectiveness by history of mental health conditions. The only exception was for vaping products, where the data favoured the null (Bayes factor = 0.20), indicating that the effectiveness of vaping products for smoking cessation did not differ significantly between those with and without a history of mental health conditions.

There was no notable difference in the pattern of results when history of mental health conditions was analysed as a 3-level variable (distinguishing between those with none, a single mental health condition, and multiple conditions; S4 Table ).

Nine in every 20 people who attempted to quit smoking had a history of one or more mental health conditions. Those with a history of mental health conditions were more likely to support their quit attempt with the use of cessation aids. Specifically, they were more likely than those without a history of mental health conditions to report using vaping products, prescription NRT, or websites, with no significant differences between groups in the use of other aids. After we adjusted for covariates and participants’ use of other cessation aids, those who used vaping products, varenicline, or heated tobacco products had significantly higher odds of quitting successfully than those who did not report using these aids. There was little evidence of benefits of using other cessation aids, or that the user’s history of mental health conditions moderated the effectiveness of any aid.

Our results echo the findings of the EAGLES trial [ 38 ], which found varenicline, bupropion, and nicotine patch were similarly effective for smokers with and without psychiatric disorders, under trial conditions. They also extend existing evidence by covering the whole range of cessation aids used by people who smoke in England and using observational data from people using these aids in the real world, where people do not necessarily receive continued monitoring and support from healthcare professionals.

The real-world effectiveness of varenicline and vaping products are established, having been reported in a number of previous studies [ 15 – 24 ]. In 2019, we used data from the Smoking Toolkit Study to examine the effectiveness of different cessation aids when used in real-world settings [ 23 ]. Our results suggested using varenicline or vaping products was associated with the highest odds of success in a quit attempt. When we controlled for use of other aids and other potential confounding variables (e.g., level of dependence), we found that people who used varenicline or vaping products in a quit attempt had 1.82- and 1.95-times higher odds, respectively, of remaining abstinent than those who did not. Our present results, which use data from the same survey but over a different time frame and with additional adjustment for history of mental health conditions, are consistent with these estimates.

However, to our knowledge, this is the first observational study to examine the effectiveness of heated tobacco products, because use of these products until recently has been rare in England [ 47 ]. We documented an association between use of heated tobacco products and increased odds of quit success [ 30 ]. Our data indicate use of these products in quit attempts remains relatively rare (consistent with low overall prevalence of use among adults in England [ 47 ]). As a result, the 95% CI around the estimate was wide and included the possibility of no meaningful difference (lower CI = 1.01), so conclusions may change with more data. It will be important to continue to monitor the effectiveness of heated tobacco products as the number of people using them to quit smoking grows.

The lack of evidence for differential effectiveness of any cessation aid by the user’s history of mental health conditions should provide reassurance to people with mental health conditions who want to stop smoking that their condition need not affect their choice of cessation aid. Of note, vaping products were both the most popular aid used by people with and without a history of mental health conditions and one of the most effective. Vaping products were also the only aid for which the data provided clear evidence that effectiveness was not lower for users with a history of mental health conditions (data for the other aids were insensitive).

Our results also suggest that healthcare professionals can base their recommendations for, and prescription of, smoking cessation treatments to people with mental health conditions on evidence of their effectiveness in the general population. Previous research has shown that people with mental health conditions have lower odds of being prescribed varenicline than NRT, despite having greater odds of quitting successfully with varenicline than NRT [ 54 ]. Consistent with this, our data show higher prevalence of use of prescription NRT among people with a history of mental health conditions than those without, and significantly higher odds of quit success among users of varenicline, but not NRT. Healthcare professionals may opt to prescribe NRT over varenicline for patients with mental health conditions due to concerns that varenicline may increase the risk of neuropsychiatric adverse events [ 55 ]. However, much evidence of this risk is based on information contained in case reports [ 55 ], and a large RCT of the relative neuropsychiatry safety of varenicline compared with nicotine patch and placebo among people with and without psychiatric disorders observed no significant increase in adverse events among those randomised to use varenicline [ 38 ]. If the risk of adverse events are similar, offering the more effective treatment (varenicline, once available again) is likely to be the better option.

This study had several limitations. First, questions on mental health conditions relied on self-reports, which may be less accurate than if linked health record data were used. Second, the items assessed ever (as opposed to current) diagnoses. As such, the results cannot tell us whether treatment effectiveness differs according to the user’s current mental health status. In addition, those with a history of multiple mental health conditions may also have been diagnosed with these conditions at different points in time, so a history of multiple mental health conditions may not reflect current comorbidity. Third, to boost statistical power for analyses, we grouped together participants reporting any of the mental health conditions we assessed. As the list of conditions was heterogeneous, covering a broad range of conditions from common mental health disorders (e.g., anxiety and depression) to severe mental illness (psychosis), we cannot rule out the possibility that certain conditions may moderate the effectiveness of cessation aids while others do not. Given the low prevalence of most of these conditions within the general population, much larger samples would be required to explore this. Fourth, despite combining all mental health conditions, Bayes factors indicated our data were insensitive to distinguish between evidence of absence of an interaction between aid use and mental health conditions (i.e., mental health conditions moderate treatment effectiveness) and absence of evidence for the majority of aids (all except vaping products). This means we are unable to conclusively rule out there being small to moderate differences in effectiveness by people’s history of mental health conditions. Fifth, although we adjusted for a range of potential confounders, there may be residual confounding by other variables not included in our models. Finally, it is possible that smoking cessation treatments offered to people with mental health conditions may differ from the general population, introducing potential selection bias from the treatment provider in addition to the user. Although clinical trials suggest varenicline and bupropion are effective for people with severe mental illness [ 38 , 56 ], in the real world, people with these conditions are rarely offered these medications by clinicians [ 54 ]. Interactions with other medications is an important consideration in deciding on a treatment approach: bupropion is known to interact with other medications (including those indicated for treatment of mental health conditions), which may reduce the effectiveness of one or both treatments [ 57 ]. Nonetheless, our data provide useful insights into potential differences in the effectiveness of popular smoking cessation treatments in a real-world setting.

In conclusion, use of vaping products, varenicline, or heated tobacco products in a quit attempt was associated with significantly greater odds of successful cessation, after adjustment for use of other cessation aids and potential confounders. There was no evidence to suggest the effectiveness of any popular cessation aid differed according to the user’s history of mental health conditions.

Supporting information

S1 table. weighted sample characteristics– 3-level mental health variable..

https://doi.org/10.1371/journal.pmen.0000007.s001

S2 Table. Use of cessation aids in the most recent quit attempt by history of mental health conditions– 3-level mental health variable.

https://doi.org/10.1371/journal.pmen.0000007.s002

S3 Table. Use of cessation aids in the most recent quit attempt by history of mental health conditions–by individual mental health condition.

https://doi.org/10.1371/journal.pmen.0000007.s003

S4 Table. Real-world effectiveness of cessation aids for success in stopping smoking and interactions with the user’s history of mental health conditions– 3-level mental health variable.

https://doi.org/10.1371/journal.pmen.0000007.s004

S1 Questionnaire. Smoking Toolkit Study questionnaire.

https://doi.org/10.1371/journal.pmen.0000007.s005

View Article
Google Scholar
PubMed/NCBI
5. Royal College of Physicians, Royal College of Psychiatrists. Smoking and mental health. London: Royal College of Physicians; 2013. Available: https://www.rcplondon.ac.uk/projects/outputs/smoking-and-mental-health
17. Kotz D, Brown J, West R. Prospective cohort study of the effectiveness of smoking cessation treatments used in the “real world.” Mayo Clinic Proceedings. Elsevier; 2014. pp. 1360–1367.

Academic Support for Nursing Students

No notifications.

Disclaimer: This essay has been written by a student and not our expert nursing writers. View professional sample essays here.

View full disclaimer

Any opinions, findings, conclusions, or recommendations expressed in this essay are those of the author and do not necessarily reflect the views of NursingAnswers.net. This essay should not be treated as an authoritative source of information when forming medical opinions as information may be inaccurate or out-of-date.

Interventions for Smoking Cessation

Info: 2555 words (10 pages) Nursing Essay Published: 11th Feb 2020

Reference this

Tagged: smoking

If you need assistance with writing your nursing essay, our professional nursing essay writing service is here to help!

Our nursing and healthcare experts are ready and waiting to assist with any writing project you may have, from simple essay plans, through to full nursing dissertations.

Cite This Work

To export a reference to this article please select a referencing stye below:

Related Services

Nursing Essay Writing Service

Nursing Dissertation Service

Female student reading and using laptop to study

Reflective Writing Service

DMCA / Removal Request

If you are the original writer of this essay and no longer wish to have your work published on the NursingAnswers.net website then please:

Our academic writing and marking services can help you!

Marking Service
Samples of our Work
Full Service Portfolio

Related Lectures

Study for free with our range of nursing lectures!

Drug Classification
Emergency Care
Health Observation
Palliative Care
Professional Values

Illustration of a nurse writing a report

Write for Us

Do you have a 2:1 degree or higher in nursing or healthcare?

Study Resources

Free resources to assist you with your nursing studies!

APA Citation Tool
Example Nursing Essays
Example Nursing Assignments
Example Nursing Case Studies
Reflective Nursing Essays
Nursing Literature Reviews
Free Resources
Reflective Model Guides
Nursing and Healthcare Pay 2021

DOI: 10.1016/j.addbeh.2024.108077
Corpus ID: 270207856

Does e-cigarette use predict short-term smoking cessation behaviors among adults who smoke in Mexico? A longitudinal study.

Katia Gallegos-Carrillo , Inti Barrientos-Gutiérrez , +5 authors James F. Thrasher
Published in Addictive Behaviours 1 June 2024

25 References

Non-pharmacological interventions for smoking cessation: analysis of systematic reviews and meta-analyses, smoking dependence, time-discounting, and sustained cessation behavior: a longitudinal study of predominantly light smokers., consumo de tabaco y uso de cigarro electrónico en adolescentes y adultos mexicanos. ensanut continua 2022, transitions between tobacco products: correlates of changes in cigarette smoking and e-cigarette use among exclusive adult smokers and dual users in mexico, electronic cigarette use among adults in 14 countries: a cross-sectional study, association of e-cigarette use with discontinuation of cigarette smoking among adult smokers who were initially never planning to quit, incidence of cigarette smoking relapse among individuals who switched to e-cigarettes or other tobacco products, revision of the wisconsin smoking withdrawal scale: development of brief and long forms., e-cigarette use and adult cigarette smoking cessation: a meta-analysis., effect of e-cigarettes plus counseling vs counseling alone on smoking cessation: a randomized clinical trial., related papers.

Showing 1 through 3 of 0 Related Papers

Nursing Interventions for Smoking Cessation Essay

To find inspiration for your paper and overcome writer’s block
As a source of information (ensure proper referencing)
As a template for you assignment

This review is titled “Nursing Interventions for Smoking Cessation” and its main objective is to find out the effectiveness of nursing-initiated smoking cessation interventions (Rice, Hartmann‐Boyce & Stead, 2013). The review was mainly authored by Virginia Rice and Lindsay Stead and both authors are notable nursing authorities in the universities of Michigan and Oxford respectively. This systematic research review is relevant to nursing because nurses are among the health practitioners who can have a major impact on patient behavior. For instance, it is common for healthcare practitioners to give advice to individuals who are trying to stop smoking. Quitting smoking is an uphill task for most individuals and this undertaking requires a lot of guidance and support. Even though the advice that nurses give to potential smokers might be brief, it can have a significant effect on smoking cessation. The authors of this review note that nurses are the most common healthcare professionals; hence, their contributions towards smoke cessation activities cannot be overlooked. The article’s research relies on forty-two clinical studies and an upward of fifteen thousand participants. The research is relevant to nursing practice because its overall finding was that nurses could help individuals in their efforts to stop smoking. In addition, the article notes that most support from the nursing staff comes in the form of advice or encouragement. Several stakeholders in the nursing profession including nurses and trainers can use the information that is provided in this article to improve their practices. Furthermore, this research can be used to reduce the rates of tobacco-related deaths in the world.

The authors of this review are able to set out their objectives in respect to their subject of study. For instance, the authors are able to recognize the need to classify the level of intensity in respect to the intervention that is employed by nurses towards smoking cessation. This strategy enables the researchers to gauge how smoking-cessation intervention can be tailored to make it more effective in future. For example, nurses can be advised to be either persistent or take a casual attitude when advising or encouraging smokers. On the other hand, the authors are positively inquisitive about the use of aids and other props when they are communicating to smokers. This approach is important and it can be used as a base for future studies in the subject of smoking cessation. The objectives of this study are simple to achieve because they are narrow-based and pinpointed to simple goals. However, the review can be faulted for failing to take a ‘complex medical’ stance through its objectives. For instance, it is clear that this systematic research review would not be useful to broader addiction subject matters such as nicotine replacement therapy.

The methods that are used in this study are quite accurate and simple. The reviewers chose to focus on the studies that had at least two treatment groups in their categorization. In addition, all the studies that were used for this review had random samples. These two approaches enable the authors to reduce their chances of working with faulty data. Consequently, the methodology that is used in this study is quite reliable. The study only used adult smokers as participants thereby avoiding the complexities that involve the issues of underage smoking. For instance, most underage smokers are not habitual smokers and they tend to keep shifting through various brands of tobacco products. The method that is used in this study is quite effective in respect to the subject matter of ‘quitting smoking’. The most important part of the methodology that is used by the study involves the authors’ choice of nurse-initiated interventions. The strategy of categorizing these interventions is important to the study’s objectives. The authors of this study categorize the advice that is given by nurses in respect to its ability to pass the ‘stop smoking’ message to patients. The study’s sampling methods are quite effective because they utilize the best available tools. For example, the reviewers utilized the Tobacco Addiction Review Group register. This register records all relevant tobacco addiction trials. The use of a professionalized register eliminates the probability of the authors of this paper working on inadequate trials. However, the data extraction techniques that are used in this study are ambiguous and clattered. The authors’ data extraction procedure involves the collection of too much or too limited information from the study’s samples. For example, the authors only record five categories of information from the studied samples. This brevity in analysis has the potential to overlook or overemphasize some pieces of information in respect to the subject matter. For instance, the authors classify the intensity of the interventions that are used for smoking cessation as either ‘high’ or ‘low’. This approach is too simplistic and it warrants for addition research when it comes to the specifics of the intensity of the intervention that is used when nurses are communicating the smoking cessation message to patients. Nevertheless, the study’s quality assessment and data analysis methods are quite effective because they are considerate of their prospective readers. Furthermore, the authors have presented a simplified glossary of the terms that are used in this study. The glossary is helpful to both the professional and non-professional users of this review.

The authors’ presentation of the results is significant and it contributes towards the realization of the study’s objectives. The authors begin by noting that all the studied forty-two trials were able to meet the criteria for this review. The results’ analysis is buoyed by the fact that all the studies took place in different places across the world. For instance, the results of the article indicate that the studies took place in the USA, UK, Canada, Japan, Denmark, Australia, Norway, and Spain. The authors are also able to account for the risk of bias by being mindful of the error factor in the randomization process. The use of computer technology in the study also minimized the error margin in respect to the big number of studies that were picked for this systematic research review. Overall, the results of this study indicated that nurse-based intervention was instrumental in helping patients to quit smoking. These results are presented in a coherent manner and the authors are able to defend them with their choice of research methodology and analysis. The authors are also able to present the results of the Systematic research review in segments that are easy to understand. For instance, the findings of this review first take to account two important considerations; the descriptions of the studies and the biases that are expected in the studies. Consequently, the readers are familiarized with the pitfalls of the reviewers before going through the study’s results.

According to the authors of this article, the results of this study indicate that nurses are important when it comes to smoking cessation. This finding is part of the ‘expected’ results. On the other hand, some of the results that are presented in this review are quite interesting. For instance, the study found that interventions that were done over the telephone had a lesser impact than the ones that were conducted face to face. This is interesting especially when the attitude of most smokers is put into account. Furthermore, even when telephone interventions were done with a higher intensity, their effects on smoking cessation were still minimal (Rice, Hartmann‐Boyce & Stead, 2013). The results of this systematic research review are hard to dispute. In addition, the authors present their findings in a simplistic manner that does not elicit additional questions in respect to the paper’s objectives. Nevertheless, the results of the study do not appeal to the top-level academics who might be interested in the specifics of smoking cessation interventions. The authors of this systematic research review utilized over forty studies when compiling their paper. However, it is apparent that the authors took time to ‘simplify’ some of these studies. This action makes some of these studies unpalatable to some academics.

The conclusions of the authors dwell a lot on the benefits that their study brings to nurses and their patients. Nevertheless, the authors take time to distance their study from the practice of Nicotine Replacement Therapy (NRT). It would have been prudent for the authors to incorporate NRT in their study because it is very closely connected to smoking cessation. All the conclusions of the authors are brief and accurate thereby offering readers the last item of satisfaction as far as this study is concerned.

Rice, V. H., Hartmann‐Boyce, J., & Stead, L. F. (2013). Nursing interventions for smoking cessation. The Cochrane Library, 1 (1), 1-60.

Smoking Cessation Treatment: The System-Level Intervention
Introducing Smoking Cessation Program: 5 A's Intervention Plan
Effectiveness of the Cognitive Behavioral Therapy for Smoking Cessation
Nursing Career: Quantitative and Qualitative Studies
Spiritual Needs Assessment of a Muslim Patient
Conditions for Medical Practice and Nursing
Nursing Shortage and Its Effects on Healthcare Delivery
Nursing Politics and Change Management
Chicago (A-D)
Chicago (N-B)

IvyPanda. (2022, April 15). Nursing Interventions for Smoking Cessation. https://ivypanda.com/essays/nursing-interventions-for-smoking-cessation/

"Nursing Interventions for Smoking Cessation." IvyPanda , 15 Apr. 2022, ivypanda.com/essays/nursing-interventions-for-smoking-cessation/.

IvyPanda . (2022) 'Nursing Interventions for Smoking Cessation'. 15 April.

IvyPanda . 2022. "Nursing Interventions for Smoking Cessation." April 15, 2022. https://ivypanda.com/essays/nursing-interventions-for-smoking-cessation/.

1. IvyPanda . "Nursing Interventions for Smoking Cessation." April 15, 2022. https://ivypanda.com/essays/nursing-interventions-for-smoking-cessation/.

Bibliography

IvyPanda . "Nursing Interventions for Smoking Cessation." April 15, 2022. https://ivypanda.com/essays/nursing-interventions-for-smoking-cessation/.

Quit Connect Helps Black Patients with Rheumatoid Arthritis Quit Smoking

An innovative program helped Black patients with rheumatoid arthritis to quit smoking, according to a new paper in Arthritis Care & Research. The program, Quit Connect (QC), prompts clinicians to refer patients to programs that help them address their smoking,

At a safety-net rheumatology clinic, QC increased cessation referrals 20-fold. When clinic staff open their electronic health records, QC prompts them to check with patients about tobacco use, advise them to address it, and connect them to counseling. QC improved tobacco screening, readiness-to-quit assessment, and referrals. QC was also feasible and cost-effective. Each quit attempt cost approximately $4 to $10.

Staff found the intervention feasible and acceptable.

During two years in this safety-net rheumatology clinic serving predominantly Black patients, 58.9% of patients indicated readiness to cut back or quit smoking when asked. Post-implementation, among 550 visits with patients who smoked, 102 people accepted a referral to either a quitline or a class to address their tobacco use.

The authors, which included UW-CTRI Research Director Dr. Megan Piper , said that, given the importance of smoking cessation to reduce cardiovascular disease and rheumatic disease burden, QC is a model for clinics across the country.

Brandt J, Ramly E, Lim SS, Bao G, Messina ML, Piper ME , Bartels CM. (2024) Implementing a Staff-Led Smoking Cessation Intervention in a Diverse Safety-Net Rheumatology Clinic: A Pre-Post Scalability Study In a Low Resource Setting . Arthritis Care & Research . Online April 15, 2024.

Warning: The NCBI web site requires JavaScript to function. more...

An official website of the United States government

The .gov means it's official. Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you're on a federal government site.

The site is secure. The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Publications
Account settings
Browse Titles

NCBI Bookshelf. A service of the National Library of Medicine, National Institutes of Health.

National Center for Chronic Disease Prevention and Health Promotion (US) Office on Smoking and Health. Preventing Tobacco Use Among Youth and Young Adults: A Report of the Surgeon General. Atlanta (GA): Centers for Disease Control and Prevention (US); 2012.

Cover of Preventing Tobacco Use Among Youth and Young Adults

Preventing Tobacco Use Among Youth and Young Adults: A Report of the Surgeon General.

1 introduction, summary, and conclusions.

Introduction

Tobacco use is a global epidemic among young people. As with adults, it poses a serious health threat to youth and young adults in the United States and has significant implications for this nation’s public and economic health in the future ( Perry et al. 1994 ; Kessler 1995 ). The impact of cigarette smoking and other tobacco use on chronic disease, which accounts for 75% of American spending on health care ( Anderson 2010 ), is well-documented and undeniable. Although progress has been made since the first Surgeon General’s report on smoking and health in 1964 ( U.S. Department of Health, Education, and Welfare [USDHEW] 1964 ), nearly one in four high school seniors is a current smoker. Most young smokers become adult smokers. One-half of adult smokers die prematurely from tobacco-related diseases ( Fagerström 2002 ; Doll et al. 2004 ). Despite thousands of programs to reduce youth smoking and hundreds of thousands of media stories on the dangers of tobacco use, generation after generation continues to use these deadly products, and family after family continues to suffer the devastating consequences. Yet a robust science base exists on social, biological, and environmental factors that influence young people to use tobacco, the physiology of progression from experimentation to addiction, other health effects of tobacco use, the epidemiology of youth and young adult tobacco use, and evidence-based interventions that have proven effective at reducing both initiation and prevalence of tobacco use among young people. Those are precisely the issues examined in this report, which aims to support the application of this robust science base.

Nearly all tobacco use begins in childhood and adolescence ( U.S. Department of Health and Human Services [USDHHS] 1994 ). In all, 88% of adult smokers who smoke daily report that they started smoking by the age of 18 years (see Chapter 3 , “The Epidemiology of Tobacco Use Among Young People in the United States and Worldwide”). This is a time in life of great vulnerability to social influences ( Steinberg 2004 ), such as those offered through the marketing of tobacco products and the modeling of smoking by attractive role models, as in movies ( Dalton et al. 2009 ), which have especially strong effects on the young. This is also a time in life of heightened sensitivity to normative influences: as tobacco use is less tolerated in public areas and there are fewer social or regular users of tobacco, use decreases among youth ( Alesci et al. 2003 ). And so, as we adults quit, we help protect our children.

Cigarettes are the only legal consumer products in the world that cause one-half of their long-term users to die prematurely ( Fagerström 2002 ; Doll et al. 2004 ). As this epidemic continues to take its toll in the United States, it is also increasing in low- and middle-income countries that are least able to afford the resulting health and economic consequences ( Peto and Lopez 2001 ; Reddy et al. 2006 ). It is past time to end this epidemic. To do so, primary prevention is required, for which our focus must be on youth and young adults. As noted in this report, we now have a set of proven tools and policies that can drastically lower youth initiation and use of tobacco products. Fully committing to using these tools and executing these policies consistently and aggressively is the most straight forward and effective to making future generations tobacco-free.

The 1994 Surgeon General’s Report

This Surgeon General’s report on tobacco is the second to focus solely on young people since these reports began in 1964. Its main purpose is to update the science of smoking among youth since the first comprehensive Surgeon General’s report on tobacco use by youth, Preventing Tobacco Use Among Young People , was published in 1994 ( USDHHS 1994 ). That report concluded that if young people can remain free of tobacco until 18 years of age, most will never start to smoke. The report documented the addiction process for young people and how the symptoms of addiction in youth are similar to those in adults. Tobacco was also presented as a gateway drug among young people, because its use generally precedes and increases the risk of using illicit drugs. Cigarette advertising and promotional activities were seen as a potent way to increase the risk of cigarette smoking among young people, while community-wide efforts were shown to have been successful in reducing tobacco use among youth. All of these conclusions remain important, relevant, and accurate, as documented in the current report, but there has been considerable research since 1994 that greatly expands our knowledge about tobacco use among youth, its prevention, and the dynamics of cessation among young people. Thus, there is a compelling need for the current report.

Tobacco Control Developments

Since 1994, multiple legal and scientific developments have altered the tobacco control environment and thus have affected smoking among youth. The states and the U.S. Department of Justice brought lawsuits against cigarette companies, with the result that many internal documents of the tobacco industry have been made public and have been analyzed and introduced into the science of tobacco control. Also, the 1998 Master Settlement Agreement with the tobacco companies resulted in the elimination of billboard and transit advertising as well as print advertising that directly targeted underage youth and limitations on the use of brand sponsorships ( National Association of Attorneys General [NAAG] 1998 ). This settlement also created the American Legacy Foundation, which implemented a nationwide antismoking campaign targeting youth. In 2009, the U.S. Congress passed a law that gave the U.S. Food and Drug Administration authority to regulate tobacco products in order to promote the public’s health ( Family Smoking Prevention and Tobacco Control Act 2009 ). Certain tobacco companies are now subject to regulations limiting their ability to market to young people. In addition, they have had to reimburse state governments (through agreements made with some states and the Master Settlement Agreement) for some health care costs. Due in part to these changes, there was a decrease in tobacco use among adults and among youth following the Master Settlement Agreement, which is documented in this current report.

Recent Surgeon General Reports Addressing Youth Issues

Other reports of the Surgeon General since 1994 have also included major conclusions that relate to tobacco use among youth ( Office of the Surgeon General 2010 ). In 1998, the report focused on tobacco use among U.S. racial/ethnic minority groups ( USDHHS 1998 ) and noted that cigarette smoking among Black and Hispanic youth increased in the 1990s following declines among all racial/ethnic groups in the 1980s; this was particularly notable among Black youth, and culturally appropriate interventions were suggested. In 2000, the report focused on reducing tobacco use ( USDHHS 2000b ). A major conclusion of that report was that school-based interventions, when implemented with community- and media-based activities, could reduce or postpone the onset of smoking among adolescents by 20–40%. That report also noted that effective regulation of tobacco advertising and promotional activities directed at young people would very likely reduce the prevalence and onset of smoking. In 2001, the Surgeon General’s report focused on women and smoking ( USDHHS 2001 ). Besides reinforcing much of what was discussed in earlier reports, this report documented that girls were more affected than boys by the desire to smoke for the purpose of weight control. Given the ongoing obesity epidemic ( Bonnie et al. 2007 ), the current report includes a more extensive review of research in this area.

The 2004 Surgeon General’s report on the health consequences of smoking ( USDHHS 2004 ) concluded that there is sufficient evidence to infer that a causal relationship exists between active smoking and (a) impaired lung growth during childhood and adolescence; (b) early onset of decline in lung function during late adolescence and early adulthood; (c) respiratory signs and symptoms in children and adolescents, including coughing, phlegm, wheezing, and dyspnea; and (d) asthma-related symptoms (e.g., wheezing) in childhood and adolescence. The 2004 Surgeon General’s report further provided evidence that cigarette smoking in young people is associated with the development of atherosclerosis.

The 2010 Surgeon General’s report on the biology of tobacco focused on the understanding of biological and behavioral mechanisms that might underlie the pathogenicity of tobacco smoke ( USDHHS 2010 ). Although there are no specific conclusions in that report regarding adolescent addiction, it does describe evidence indicating that adolescents can become dependent at even low levels of consumption. Two studies ( Adriani et al. 2003 ; Schochet et al. 2005 ) referenced in that report suggest that because the adolescent brain is still developing, it may be more susceptible and receptive to nicotine than the adult brain.

Scientific Reviews

Since 1994, several scientific reviews related to one or more aspects of tobacco use among youth have been undertaken that also serve as a foundation for the current report. The Institute of Medicine (IOM) ( Lynch and Bonnie 1994 ) released Growing Up Tobacco Free: Preventing Nicotine Addiction in Children and Youths, a report that provided policy recommendations based on research to that date. In 1998, IOM provided a white paper, Taking Action to Reduce Tobacco Use, on strategies to reduce the increasing prevalence (at that time) of smoking among young people and adults. More recently, IOM ( Bonnie et al. 2007 ) released a comprehensive report entitled Ending the Tobacco Problem: A Blueprint for the Nation . Although that report covered multiple potential approaches to tobacco control, not just those focused on youth, it characterized the overarching goal of reducing smoking as involving three distinct steps: “reducing the rate of initiation of smoking among youth (IOM [ Lynch and Bonnie] 1994 ), reducing involuntary tobacco smoke exposure ( National Research Council 1986 ), and helping people quit smoking” (p. 3). Thus, reducing onset was seen as one of the primary goals of tobacco control.

As part of USDHHS continuing efforts to assess the health of the nation, prevent disease, and promote health, the department released, in 2000, Healthy People 2010 and, in 2010, Healthy People 2020 ( USDHHS 2000a , 2011 ). Healthy People provides science-based, 10-year national objectives for improving the health of all Americans. For 3 decades, Healthy People has established benchmarks and monitored progress over time in order to encourage collaborations across sectors, guide individuals toward making informed health decisions, and measure the impact of prevention activities. Each iteration of Healthy People serves as the nation’s disease prevention and health promotion roadmap for the decade. Both Healthy People 2010 and Healthy People 2020 highlight “Tobacco Use” as one of the nation’s “Leading Health Indicators,” feature “Tobacco Use” as one of its topic areas, and identify specific measurable tobacco-related objectives and targets for the nation to strive for. Healthy People 2010 and Healthy People 2020 provide tobacco objectives based on the most current science and detailed population-based data to drive action, assess tobacco use among young people, and identify racial and ethnic disparities. Additionally, many of the Healthy People 2010 and 2020 tobacco objectives address reductions of tobacco use among youth and target decreases in tobacco advertising in venues most often influencing young people. A complete list of the healthy people 2020 objectives can be found on their Web site ( USDHHS 2011 ).

In addition, the National Cancer Institute (NCI) of the National Institutes of Health has published monographs pertinent to the topic of tobacco use among youth. In 2001, NCI published Monograph 14, Changing Adolescent Smoking Prevalence , which reviewed data on smoking among youth in the 1990s, highlighted important statewide intervention programs, presented data on the influence of marketing by the tobacco industry and the pricing of cigarettes, and examined differences in smoking by racial/ethnic subgroup ( NCI 2001 ). In 2008, NCI published Monograph 19, The Role of the Media in Promoting and Reducing Tobacco Use ( NCI 2008 ). Although young people were not the sole focus of this Monograph, the causal relationship between tobacco advertising and promotion and increased tobacco use, the impact on youth of depictions of smoking in movies, and the success of media campaigns in reducing youth tobacco use were highlighted as major conclusions of the report.

The Community Preventive Services Task Force (2011) provides evidence-based recommendations about community preventive services, programs, and policies on a range of topics including tobacco use prevention and cessation ( Task Force on Community Preventive Services 2001 , 2005 ). Evidence reviews addressing interventions to reduce tobacco use initiation and restricting minors’ access to tobacco products were cited and used to inform the reviews in the current report. The Cochrane Collaboration (2010) has also substantially contributed to the review literature on youth and tobacco use by producing relevant systematic assessments of health-related programs and interventions. Relevant to this Surgeon General’s report are Cochrane reviews on interventions using mass media ( Sowden 1998 ), community interventions to prevent smoking ( Sowden and Stead 2003 ), the effects of advertising and promotional activities on smoking among youth ( Lovato et al. 2003 , 2011 ), preventing tobacco sales to minors ( Stead and Lancaster 2005 ), school-based programs ( Thomas and Perara 2006 ), programs for young people to quit using tobacco ( Grimshaw and Stanton 2006 ), and family programs for preventing smoking by youth ( Thomas et al. 2007 ). These reviews have been cited throughout the current report when appropriate.

In summary, substantial new research has added to our knowledge and understanding of tobacco use and control as it relates to youth since the 1994 Surgeon General’s report, including updates and new data in subsequent Surgeon General’s reports, in IOM reports, in NCI Monographs, and in Cochrane Collaboration reviews, in addition to hundreds of peer-reviewed publications, book chapters, policy reports, and systematic reviews. Although this report is a follow-up to the 1994 report, other important reviews have been undertaken in the past 18 years and have served to fill the gap during an especially active and important time in research on tobacco control among youth.

Focus of the Report

Young People

This report focuses on “young people.” In general, work was reviewed on the health consequences, epidemiology, etiology, reduction, and prevention of tobacco use for those in the young adolescent (11–14 years of age), adolescent (15–17 years of age), and young adult (18–25 years of age) age groups. When possible, an effort was made to be specific about the age group to which a particular analysis, study, or conclusion applies. Because hundreds of articles, books, and reports were reviewed, however, there are, unavoidably, inconsistencies in the terminology used. “Adolescents,” “children,” and “youth” are used mostly interchangeably throughout this report. In general, this group encompasses those 11–17 years of age, although “children” is a more general term that will include those younger than 11 years of age. Generally, those who are 18–25 years old are considered young adults (even though, developmentally, the period between 18–20 years of age is often labeled late adolescence), and those 26 years of age or older are considered adults.

In addition, it is important to note that the report is concerned with active smoking or use of smokeless tobacco on the part of the young person. The report does not consider young people’s exposure to secondhand smoke, also referred to as involuntary or passive smoking, which was discussed in the 2006 report of the Surgeon General ( USDHHS 2006 ). Additionally, the report does not discuss research on children younger than 11 years old; there is very little evidence of tobacco use in the United States by children younger than 11 years of age, and although there may be some predictors of later tobacco use in those younger years, the research on active tobacco use among youth has been focused on those 11 years of age and older.

Tobacco Use

Although cigarette smoking is the most common form of tobacco use in the United States, this report focuses on other forms as well, such as using smokeless tobacco (including chew and snuff) and smoking a product other than a cigarette, such as a pipe, cigar, or bidi (tobacco wrapped in tendu leaves). Because for young people the use of one form of tobacco has been associated with use of other tobacco products, it is particularly important to monitor all forms of tobacco use in this age group. The term “tobacco use” in this report indicates use of any tobacco product. When the word “smoking” is used alone, it refers to cigarette smoking.

Organization of the Report

This chapter begins by providing a short synopsis of other reports that have addressed smoking among youth and, after listing the major conclusions of this report, will end by presenting conclusions specific to each chapter. Chapter 2 of this report (“The Health Consequences of Tobacco Use Among Young People”) focuses on the diseases caused by early tobacco use, the addiction process, the relation of body weight to smoking, respiratory and pulmonary problems associated with tobacco use, and cardiovascular effects. Chapter 3 (“The Epidemiology of Tobacco Use Among Young People in the United States and Worldwide”) provides recent and long-term cross-sectional and longitudinal data on cigarette smoking, use of smokeless tobacco, and the use of other tobacco products by young people, by racial/ethnic group and gender, primarily in the United States, but including some worldwide data as well. Chapter 4 (“Social, Environmental, Cognitive, and Genetic Influences on the Use of Tobacco Among Youth”) identifies the primary risk factors associated with tobacco use among youth at four levels, including the larger social and physical environments, smaller social groups, cognitive factors, and genetics and neurobiology. Chapter 5 (“The Tobacco Industry’s Influences on the Use of Tobacco Among Youth”) includes data on marketing expenditures for the tobacco industry over time and by category, the effects of cigarette advertising and promotional activities on young people’s smoking, the effects of price and packaging on use, the use of the Internet and movies to market tobacco products, and an evaluation of efforts by the tobacco industry to prevent tobacco use among young people. Chapter 6 (“Efforts to Prevent and Reduce Tobacco Use Among Young People”) provides evidence on the effectiveness of family-based, clinic-based, and school-based programs, mass media campaigns, regulatory and legislative approaches, increased cigarette prices, and community and statewide efforts in the fight against tobacco use among youth. Chapter 7 (“A Vision for Ending the Tobacco Epidemic”) points to next steps in preventing and reducing tobacco use among young people.

Preparation of the Report

This report of the Surgeon General was prepared by the Office on Smoking and Health (OSH), National Center for Chronic Disease Prevention and Health Promotion, Centers for Disease Control and Prevention (CDC), USDHHS. In 2008, 18 external independent scientists reviewed the 1994 report and suggested areas to be added and updated. These scientists also suggested chapter editors and a senior scientific editor, who were contacted by OSH. Each chapter editor named external scientists who could contribute, and 33 content experts prepared draft sections. The draft sections were consolidated into chapters by the chapter editors and then reviewed by the senior scientific editor, with technical editing performed by CDC. The chapters were sent individually to 34 peer reviewers who are experts in the areas covered and who reviewed the chapters for scientific accuracy and comprehensiveness. The entire manuscript was then sent to more than 25 external senior scientists who reviewed the science of the entire document. After each review cycle, the drafts were revised by the chapter and senior scientific editor on the basis of the experts’ comments. Subsequently, the report was reviewed by various agencies within USDHHS. Publication lags prevent up-to-the-minute inclusion of all recently published articles and data, and so some more recent publications may not be cited in this report.

Evaluation of the Evidence

Since the first Surgeon General’s report in 1964 on smoking and health ( USDHEW 1964 ), major conclusions concerning the conditions and diseases caused by cigarette smoking and the use of smokeless tobacco have been based on explicit criteria for causal inference ( USDHHS 2004 ). Although a number of different criteria have been proposed for causal inference since the 1960s, this report focuses on the five commonly accepted criteria that were used in the original 1964 report and that are discussed in greater detail in the 2004 report on the health consequences of smoking ( USDHHS 2004 ). The five criteria refer to the examination of the association between two variables, such as a risk factor (e.g., smoking) and an outcome (e.g., lung cancer). Causal inference between these variables is based on (1) the consistency of the association across multiple studies; this is the persistent finding of an association in different persons, places, circumstances, and times; (2) the degree of the strength of association, that is, the magnitude and statistical significance of the association in multiple studies; (3) the specificity of the association to clearly demonstrate that tobacco use is robustly associated with the condition, even if tobacco use has multiple effects and multiple causes exist for the condition; (4) the temporal relationship of the association so that tobacco use precedes disease onset; and (5) the coherence of the association, that is, the argument that the association makes scientific sense, given data from other sources and understanding of biological and psychosocial mechanisms ( USDHHS 2004 ). Since the 2004 Surgeon General’s report, The Health Consequences of Smoking , a four-level hierarchy ( Table 1.1 ) has been used to assess the research data on associations discussed in these reports ( USDHHS 2004 ). In general, this assessment was done by the chapter editors and then reviewed as appropriate by peer reviewers, senior scientists, and the scientific editors. For a relationship to be considered sufficient to be characterized as causal, multiple studies over time provided evidence in support of each criteria.

Four-level hierarchy for classifying the strength of causal inferences based on available evidence.

When a causal association is presented in the chapter conclusions in this report, these four levels are used to describe the strength of the evidence of the association, from causal (1) to not causal (4). Within the report, other terms are used to discuss the evidence to date (i.e., mixed, limited, and equivocal evidence), which generally represent an inadequacy of data to inform a conclusion.

However, an assessment of a casual relationship is not utilized in presenting all of the report’s conclusions. The major conclusions are written to be important summary statements that are easily understood by those reading the report. Some conclusions, particularly those found in Chapter 3 (epidemiology), provide observations and data related to tobacco use among young people, and are generally not examinations of causal relationships. For those conclusions that are written using the hierarchy above, a careful and extensive review of the literature has been undertaken for this report, based on the accepted causal criteria ( USDHHS 2004 ). Evidence that was characterized as Level 1 or Level 2 was prioritized for inclusion as chapter conclusions.

In additional to causal inferences, statistical estimation and hypothesis testing of associations are presented. For example, confidence intervals have been added to the tables in the chapter on the epidemiology of youth tobacco use (see Chapter 3 ), and statistical testing has been conducted for that chapter when appropriate. The chapter on efforts to prevent tobacco use discusses the relative improvement in tobacco use rates when implementing one type of program (or policy) versus a control program. Statistical methods, including meta-analytic methods and longitudinal trajectory analyses, are also presented to ensure that the methods of evaluating data are up to date with the current cutting-edge research that has been reviewed. Regardless of the methods used to assess significance, the five causal criteria discussed above were applied in developing the conclusions of each chapter and the report.

Major Conclusions
Cigarette smoking by youth and young adults has immediate adverse health consequences, including addiction, and accelerates the development of chronic diseases across the full life course.
Prevention efforts must focus on both adolescents and young adults because among adults who become daily smokers, nearly all first use of cigarettes occurs by 18 years of age (88%), with 99% of first use by 26 years of age.
Advertising and promotional activities by tobacco companies have been shown to cause the onset and continuation of smoking among adolescents and young adults.
After years of steady progress, declines in the use of tobacco by youth and young adults have slowed for cigarette smoking and stalled for smokeless tobacco use.
Coordinated, multicomponent interventions that combine mass media campaigns, price increases including those that result from tax increases, school-based policies and programs, and statewide or community-wide changes in smoke-free policies and norms are effective in reducing the initiation, prevalence, and intensity of smoking among youth and young adults.
Chapter Conclusions

The following are the conclusions presented in the substantive chapters of this report.

Chapter 2. The Health Consequences of Tobacco Use Among Young People

The evidence is sufficient to conclude that there is a causal relationship between smoking and addiction to nicotine, beginning in adolescence and young adulthood.
The evidence is suggestive but not sufficient to conclude that smoking contributes to future use of marijuana and other illicit drugs.
The evidence is suggestive but not sufficient to conclude that smoking by adolescents and young adults is not associated with significant weight loss, contrary to young people’s beliefs.
The evidence is sufficient to conclude that there is a causal relationship between active smoking and both reduced lung function and impaired lung growth during childhood and adolescence.
The evidence is sufficient to conclude that there is a causal relationship between active smoking and wheezing severe enough to be diagnosed as asthma in susceptible child and adolescent populations.
The evidence is sufficient to conclude that there is a causal relationship between smoking in adolescence and young adulthood and early abdominal aortic atherosclerosis in young adults.
The evidence is suggestive but not sufficient to conclude that there is a causal relationship between smoking in adolescence and young adulthood and coronary artery atherosclerosis in adulthood.

Chapter 3. The Epidemiology of Tobacco Use Among Young People in the United States and Worldwide

Among adults who become daily smokers, nearly all first use of cigarettes occurs by 18 years of age (88%), with 99% of first use by 26 years of age.
Almost one in four high school seniors is a current (in the past 30 days) cigarette smoker, compared with one in three young adults and one in five adults. About 1 in 10 high school senior males is a current smokeless tobacco user, and about 1 in 5 high school senior males is a current cigar smoker.
Among adolescents and young adults, cigarette smoking declined from the late 1990s, particularly after the Master Settlement Agreement in 1998. This decline has slowed in recent years, however.
Significant disparities in tobacco use remain among young people nationwide. The prevalence of cigarette smoking is highest among American Indians and Alaska Natives, followed by Whites and Hispanics, and then Asians and Blacks. The prevalence of cigarette smoking is also highest among lower socioeconomic status youth.
Use of smokeless tobacco and cigars declined in the late 1990s, but the declines appear to have stalled in the last 5 years. The latest data show the use of smokeless tobacco is increasing among White high school males, and cigar smoking may be increasing among Black high school females.
Concurrent use of multiple tobacco products is prevalent among youth. Among those who use tobacco, nearly one-third of high school females and more than one-half of high school males report using more than one tobacco product in the last 30 days.
Rates of tobacco use remain low among girls relative to boys in many developing countries, however, the gender gap between adolescent females and males is narrow in many countries around the globe.

Chapter 4. Social, Environmental, Cognitive, and Genetic Influences on the Use of Tobacco Among Youth

Given their developmental stage, adolescents and young adults are uniquely susceptible to social and environmental influences to use tobacco.
Socioeconomic factors and educational attainment influence the development of youth smoking behavior. The adolescents most likely to begin to use tobacco and progress to regular use are those who have lower academic achievement.
The evidence is sufficient to conclude that there is a causal relationship between peer group social influences and the initiation and maintenance of smoking behaviors during adolescence.
Affective processes play an important role in youth smoking behavior, with a strong association between youth smoking and negative affect.
The evidence is suggestive that tobacco use is a heritable trait, more so for regular use than for onset. The expression of genetic risk for smoking among young people may be moderated by small-group and larger social-environmental factors.

Chapter 5. The Tobacco Industry’s Influences on the Use of Tobacco Among Youth

In 2008, tobacco companies spent $9.94 billion on the marketing of cigarettes and $547 million on the marketing of smokeless tobacco. Spending on cigarette marketing is 48% higher than in 1998, the year of the Master Settlement Agreement. Expenditures for marketing smokeless tobacco are 277% higher than in 1998.
Tobacco company expenditures have become increasingly concentrated on marketing efforts that reduce the prices of targeted tobacco products. Such expenditures accounted for approximately 84% of cigarette marketing and more than 77% of the marketing of smokeless tobacco products in 2008.
The evidence is sufficient to conclude that there is a causal relationship between advertising and promotional efforts of the tobacco companies and the initiation and progression of tobacco use among young people.
The evidence is suggestive but not sufficient to conclude that tobacco companies have changed the packaging and design of their products in ways that have increased these products’ appeal to adolescents and young adults.
The tobacco companies’ activities and programs for the prevention of youth smoking have not demonstrated an impact on the initiation or prevalence of smoking among young people.
The evidence is sufficient to conclude that there is a causal relationship between depictions of smoking in the movies and the initiation of smoking among young people.

Chapter 6. Efforts to Prevent and Reduce Tobacco Use Among Young People

The evidence is sufficient to conclude that mass media campaigns, comprehensive community programs, and comprehensive statewide tobacco control programs can prevent the initiation of tobacco use and reduce its prevalence among youth.
The evidence is sufficient to conclude that increases in cigarette prices reduce the initiation, prevalence, and intensity of smoking among youth and young adults.
The evidence is sufficient to conclude that school-based programs with evidence of effectiveness, containing specific components, can produce at least short-term effects and reduce the prevalence of tobacco use among school-aged youth.
Adriani W, Spijker S, Deroche-Gamonet V, Laviola G, Le Moal M, Smit AB, Piazza PV. Evidence for enhanced neurobehavioral vulnerability to nicotine during peri-adolescence in rats. Journal of Neuroscience. 2003; 23 (11):4712–6. [ PMC free article : PMC6740776 ] [ PubMed : 12805310 ]
Alesci NL, Forster JL, Blaine T. Smoking visibility, perceived acceptability, and frequency in various locations among youth and adults. Preventive Medicine. 2003; 36 (3):272–81. [ PubMed : 12634018 ]
Anderson G. Chronic Care: Making the Case for Ongoing Care. Princeton (NJ): Robert Wood Johnson Foundation; 2010. [accessed: November 30, 2011]. < http://www .rwjf.org/files /research/50968chronic .care.chartbook.pdf >.
Bonnie RJ, Stratton K, Wallace RB, editors. Ending the Tobacco Problem: A Blueprint for the Nation. Washington: National Academies Press; 2007.
Cochrane Collaboration. Home page. 2010. [accessed: November 30, 2010]. < http://www .cochrane.org/ >.
Community Preventive Services Task Force. First Annual Report to Congress and to Agencies Related to the Work of the Task Force. Community Preventive Services Task Force. 2011. [accessed: January 9, 2012]. < http://www .thecommunityguide .org/library /ARC2011/congress-report-full.pdf >.
Dalton MA, Beach ML, Adachi-Mejia AM, Longacre MR, Matzkin AL, Sargent JD, Heatherton TF, Titus-Ernstoff L. Early exposure to movie smoking predicts established smoking by older teens and young adults. Pediatrics. 2009; 123 (4):e551–e558. [ PMC free article : PMC2758519 ] [ PubMed : 19336346 ]
Doll R, Peto R, Boreham J, Sutherland I. Mortality in relation to smoking: 50 years’ observations on male British doctors. BMJ (British Medical Journal). 2004; 32 :1519. [ PMC free article : PMC437139 ] [ PubMed : 15213107 ] [ CrossRef ]
Fagerström K. The epidemiology of smoking: health consequences and benefits of cessation. Drugs. 2002; 62 (Suppl 2):1–9. [ PubMed : 12109931 ]
Family Smoking Prevention and Tobacco Control Act, Public Law 111-31, 123 U.S. Statutes at Large 1776 (2009)
Grimshaw G, Stanton A. Tobacco cessation interventions for young people. Cochrane Database of Systematic Reviews. 2006;(4):CD003289. [ PubMed : 17054164 ] [ CrossRef ]
Kessler DA. Nicotine addiction in young people. New England Journal of Medicine. 1995; 333 (3):186–9. [ PubMed : 7791824 ]
Lovato C, Linn G, Stead LF, Best A. Impact of tobacco advertising and promotion on increasing adolescent smoking behaviours. Cochrane Database of Systematic Reviews. 2003;(4):CD003439. [ PubMed : 14583977 ] [ CrossRef ]
Lovato C, Watts A, Stead LF. Impact of tobacco advertising and promotion on increasing adolescent smoking behaviours. Cochrane Database of Systematic Reviews. 2011;(10):CD003439. [ PMC free article : PMC7173757 ] [ PubMed : 21975739 ] [ CrossRef ]
Lynch BS, Bonnie RJ, editors. Growing Up Tobacco Free: Preventing Nicotine Addiction in Children and Youths. Washington: National Academies Press; 1994. [ PubMed : 25144107 ]
National Association of Attorneys General. Master Settlement Agreement. 1998. [accessed: June 9, 2011]. < http://www .naag.org/back-pages /naag/tobacco /msa/msa-pdf/MSA%20with %20Sig%20Pages%20and%20Exhibits .pdf/file_view >.
National Cancer Institute. Changing Adolescent Smoking Prevalence. Bethesda (MD): U.S. Department of Health and Human Services, Public Health Service, National Institutes of Health, National Cancer Institute; 2001. Smoking and Tobacco Control Monograph No. 14. NIH Publication. No. 02-5086.
National Cancer Institute. The Role of the Media in Promoting and Reducing Tobacco Use. Bethesda (MD): U.S. Department of Health and Human Services, National Institutes of Health, National Cancer Institute; 2008. Tobacco Control Monograph No. 19. NIH Publication No. 07-6242.
National Research Council. Environmental Tobacco Smoke: Measuring Exposures and Assessing Health Effects. Washington: National Academy Press; 1986. [ PubMed : 25032469 ]
Office of the Surgeon General Reports of the Surgeon General, U.S. Public Health Service. 2010. [accessed: November 30, 2010]. < http://www .surgeongeneral .gov/library/reports/index.html >.
Perry CL, Eriksen M, Giovino G. Tobacco use: a pediatric epidemic [editorial] Tobacco Control. 1994; 3 (2):97–8.
Peto R, Lopez AD. Future worldwide health effects of current smoking patterns. In: Koop CE, Pearson CE, Schwarz MR, editors. Critical Issues in Global Health. San Francisco: Wiley (Jossey-Bass); 2001. pp. 154–61.
Reddy KS, Perry CL, Stigler MH, Arora M. Differences in tobacco use among young people in urban India by sex, socioeconomic status, age, and school grade: assessment of baseline survey data. Lancet. 2006; 367 (9510):589–94. [ PubMed : 16488802 ]
Schochet TL, Kelley AE, Landry CF. Differential expression of arc mRNA and other plasticity-related genes induced by nicotine in adolescent rat forebrain. Neuroscience. 2005; 135 (1):285–97. [ PMC free article : PMC1599838 ] [ PubMed : 16084664 ]
Sowden AJ. Mass media interventions for preventing smoking in young people. Cochrane Database of Systematic Reviews. 1998;(4):CD001006. [ PubMed : 10796581 ] [ CrossRef ]
Sowden AJ, Stead LF. Community interventions for preventing smoking in young people. Cochrane Database of Systematic Reviews. 2003;(1):CD001291. [ PubMed : 12535406 ] [ CrossRef ]
Stead LF, Lancaster T. Interventions for preventing tobacco sales to minors. Cochrane Database of Systematic Reviews. 2005;(1):CD001497. [ PubMed : 15674880 ] [ CrossRef ]
Steinberg L. Risk taking in adolescence: what changes, and why? Annals of the New York Academy of Sciences. 2004; 1021 :51–8. [ PubMed : 15251873 ]
Task Force on Community Preventive Services. Recommendations regarding interventions to reduce tobacco use and exposure to environmental tobacco smoke. American Journal of Preventive Medicine. 2001; 20 (2 Suppl):S10–S15. [ PubMed : 11173214 ]
Task Force on Community Preventive Services. Tobacco. In: Zaza S, Briss PA, Harris KW, editors. The Guide to Preventive Services: What Works to Promote Health? New York: Oxford University Press; 2005. pp. 3–79. < http://www .thecommunityguide .org/tobacco/Tobacco.pdf >.
Thomas RE, Baker PRA, Lorenzetti D. Family-based programmes for preventing smoking by children and adolescents. Cochrane Database of Systematic Reviews. 2007;(1):CD004493. [ PubMed : 17253511 ] [ CrossRef ]
Thomas RE, Perera R. School-based programmes for preventing smoking. Cochrane Database of Systematic Reviews. 2006;(3):CD001293. [ PubMed : 16855966 ] [ CrossRef ]
US Department of Health and Human Services. Preventing Tobacco Use Among Young People A Report of the Surgeon General. Atlanta (GA): US Department of Health and Human Services, Public Health Service, Centers for Disease Control and Prevention, National Center for Chronic Disease Prevention and Health Promotion, Office on Smoking and Health; 1994.
US Department of Health and Human Services. Tobacco Use Among US Racial/Ethnic Minority Groups—African Americans, American Indians and Alaska Natives, Asian Americans and Pacific Islanders, and Hispanics A Report of the Surgeon General. Atlanta (GA): U.S. Department of Health and Human Services, Centers for Disease Control and Prevention, National Center for Chronic Disease Prevention and Health Promotion, Office on Smoking and Health; 1998.
U.S. Department of Health and Human Services. Healthy People 2010: Understanding and Improving Health. 2nd ed. Washington: U.S. Government Printing Office; 2000.
US Department of Health and Human Services. Reducing Tobacco Use: A Report of the Surgeon General. Atlanta (GA): U.S. Department of Health and Human Services, Centers for Disease Control and Prevention, National Center for Chronic Disease Prevention and Health Promotion, Office on Smoking and Health; 2000.
US Department of Health and Human Services. Women and Smoking A Report of the Surgeon General. Rockville (MD): U.S. Department of Health and Human Services, Public Health Service, Office of the Surgeon General; 2001.
US Department of Health and Human Services. The Health Consequences of Smoking: A Report of the Surgeon General. Atlanta (GA): U.S. Department of Health and Human Services, Centers for Disease Control and Prevention, National Center for Chronic Disease Prevention and Health Promotion, Office on Smoking and Health; 2004.
US Department of Health and Human Services. The Health Consequences of Involuntary Exposure to Tobacco Smoke: A Report of the Surgeon General. Atlanta (GA): U.S. Department of Health and Human Services, Centers for Disease Control and Prevention, National Center for Chronic Disease Prevention and Health Promotion, Office on Smoking and Health; 2006. [ PubMed : 20669524 ]
US Department of Health and Human Services. How Tobacco Smoke Causes Disease—The Biology and Behavioral Basis for Tobacco-Attributable Disease: A Report of the Surgeon General. Atlanta (GA): U.S. Department of Health and Human Services, Centers for Disease Control and Prevention, National Center for Chronic Disease Prevention and Health Promotion, Office on Smoking and Health; 2010. [ PubMed : 21452462 ]
U.S. Department of Health and Human Services, Office of Disease Prevention and Health Promotion. Healthy People 2020. 2011. [accessed: November 1, 2011]. < http://www .healthypeople .gov/2020/default.aspx >.
US Department of Health, Education, and Welfare. Smoking and Health: Report of the Advisory Committee to the Surgeon General of the Public Health Service. Washington: U.S. Department of Health, Education, and Welfare, Public Health Service, Center for Disease Control; 1964. PHS Publication No. 1103.
Cite this Page National Center for Chronic Disease Prevention and Health Promotion (US) Office on Smoking and Health. Preventing Tobacco Use Among Youth and Young Adults: A Report of the Surgeon General. Atlanta (GA): Centers for Disease Control and Prevention (US); 2012. 1, Introduction, Summary, and Conclusions.
PDF version of this title (18M)

In this Page

Other titles in these collections.

Reports of the Surgeon General
Health Services/Technology Assessment Text (HSTAT)

Related information

PMC PubMed Central citations
PubMed Links to PubMed

Recent Activity

Introduction, Summary, and Conclusions - Preventing Tobacco Use Among Youth and ... Introduction, Summary, and Conclusions - Preventing Tobacco Use Among Youth and Young Adults

Your browsing activity is empty.

Activity recording is turned off.

Turn recording back on

Connect with NLM

National Library of Medicine 8600 Rockville Pike Bethesda, MD 20894

Web Policies FOIA HHS Vulnerability Disclosure

Help Accessibility Careers

Research article
Open access
Published: 28 April 2023

Cross-talks between gut microbiota and tobacco smoking: a two-sample Mendelian randomization study

Jiayao Fan 1 , 2 na1 ,
Yuan Zhou 3 na1 ,
Ran Meng 1 ,
Jinsong Tang 4 ,
Jiahao Zhu 2 ,
Melinda C. Aldrich 5 , 6 ,
Nancy J. Cox 5 , 6 ,
Yimin Zhu 7 ,
Yingjun Li 2 &
Dan Zhou 1 , 8

BMC Medicine volume 21 , Article number: 163 ( 2023 ) Cite this article

13k Accesses

19 Citations

1 Altmetric

Metrics details

Considerable evidence has been reported that tobacco use could cause alterations in gut microbiota composition. The microbiota-gut–brain axis also in turn hinted at a possible contribution of the gut microbiota to smoking. However, population-level studies with a higher evidence level for causality are lacking.

This study utilized the summary-level data of respective genome-wide association study (GWAS) for 211 gut microbial taxa and five smoking phenotypes to reveal the causal association between the gut microbiota and tobacco smoking. Two-sample bidirectional Mendelian randomization (MR) design was deployed and comprehensively sensitive analyses were followed to validate the robustness of results. We further performed multivariable MR to evaluate the effect of neurotransmitter-associated metabolites on observed associations.

Our univariable MR results confirmed the effects of smoking on three taxa ( Intestinimonas , Catenibacterium , and Ruminococcaceae , observed from previous studies) with boosted evidence level and identified another 13 taxa which may be causally affected by tobacco smoking. As for the other direction, we revealed that smoking behaviors could be potential consequence of specific taxa abundance. Combining with existing observational evidence, we provided novel insights regarding a positive feedback loop of smoking through Actinobacteria and indicated a potential mechanism for the link between parental smoking and early smoking initiation of their children driven by Bifidobacterium . The multivariable MR results suggested that neurotransmitter-associated metabolites (tryptophan and tyrosine, also supported by previous studies) probably played a role in the action pathway from the gut microbiota to smoking, especially for Actinobacteria and Peptococcus .

Conclusions

In summary, the current study suggested the role of the specific gut microbes on the risk for cigarette smoking (likely involving alterations in metabolites) and in turn smoking on specific gut microbes. Our findings highlighted the hazards of tobacco use for gut flora dysbiosis and shed light on the potential role of specific gut microbiota for smoking behaviors.

Peer Review reports

Cigarette smoking, a major public health threat across the world, causes more than 8 million deaths globally each year. Despite higher awareness of cigarettes’ adverse effects and ongoing efforts on tobacco control, there still exist 22.3% of the global population being regular smokers (made up of 36.7% of the world’s men and 7.8% of all women) [ 1 ]. Smoking is highly inherited with an estimated heritability of 44% (66% for males and 21% for females, respectively) [ 2 , 3 ] and meanwhile is influenced by postnatal environmental conditions (e.g., socioeconomic position, culture). Understanding the modifiable risk factors of smoking as well as its full spectrum of consequence is always an essential and challenging question, especially at the microscale and molecular levels. The term “gut microbiota” refers to all microorganisms that inhabit the human gastrointestinal tract, whose volume reaches trillion level [ 4 ]. Due to its intricate and reciprocal symbiotic relationship with the host, the gut microbiota is closely related to human health, not just intestinal diseases [ 5 , 6 , 7 ]. The diversity and quantity of intestinal microbiome are in a dynamic balance, which might be disturbed by various factors, such as genetics, aging, living habits, as well as environmental factors (e.g., cigarette smoke exposure) [ 8 , 9 ]. Indeed, mounting observational evidence has reported that tobacco use was associated with alterations in the gut microbiota composition [ 10 , 11 , 12 ]. Taking Bifidobacterium (the representative bacteria of probiotics) for example, existing population studies unanimously found that the abundance of Bifidobacterium was significantly decreased in current smokers compared with non-smokers, regardless of the ethnicities [ 13 , 14 , 15 , 16 , 17 ]. Instead, smoking cessation, even for short periods, could somewhat restore Bifidobacterium abundance [ 15 ]. In vivo and in vitro studies [ 18 , 19 ] also supported the inhibitory effect of cigarette smoke on the growth of Bifidobacterium . However, population-level studies with higher evidence levels for causality are lacking.

Given the essential role of the gut microbiota in the regulation of the central nervous system (CNS) [ 20 ], another interesting question is whether smoking behaviors are affected by the gut microbiota. Currently, the microbiota-gut–brain axis, i.e., gut microbiota changes may alter brain function, piqued significant research interest [ 21 ]. A recent review summarized the evidence for the presence of bidirectional communications of the axis, and such crosstalk has been linked to major depressive disorder and other psychiatric disorders [ 22 ]. Another recent study also identified that abundant genetic signals associated with the gut microbiome were enriched in the genes of neurological functions [ 23 ]. In the meantime, the neurological function of the brain was further closely related to tobacco use. Two brain areas, the orbitofrontal cortex and the prefrontal cortex, could interact to turn nicotine cravings on or off [ 24 , 25 ]. The dopamine reward circuit in the limbic system of the brain was a widely accepted mechanism of tobacco use that withdrawal from nicotine, the main component of cigarettes, will cause a drastic decrease in dopamine secretion. Moreover, animal studies have directly shown that altering the gut microbiome could affect the reward- and stress-related behavior associated with substance abuse, including tobacco [ 26 , 27 , 28 ]. Therefore, the gut microbiota has the possibility to affect smoking though the pathways of microbiota-gut-brain-smoking and on the contrary gut microbial homeostasis could be a potential target for addressing tobacco use via improving brain functions [ 29 ]. However, the direct links from the microbiome to smoking behaviors which concordance with the gut-brain axis were largely unexplored.

Meanwhile, prior evidence has been found that the manner of communication between the microbiota and the brain involves autonomic nervous system with corresponding neurotransmitters (e.g., γ-aminobutyric acid (GABA), endorphins), bacterial metabolites (typically, short-chain fatty acids) [ 21 ], etc. Amino acid metabolites and amino acid-related derivatives are essential sources of most important neurotransmitters. Therefore, associations between the microbiome and smoking could be bridged by relevant metabolites, such as tryptophan (the raw material for serotonin, as known as 5-hydroxytryptamine, 5HT).

Mendelian randomization (MR) is an increasingly used approach to integrate summary data of genome-wide association study (GWAS) to identify causal links between exposures and outcomes. The main reason for its advantage in inferring causality is that MR employs the genetic variants as instrumental variables. MR uses the facts that (1) genetic variants are randomly inherit one allele from each of the father and mother (namely the law of segregation assortment) and (2) alleles will be passed to offspring independently of each other (namely the law of independent assortment). Therefore, MR results are unlikely to be influenced by the environment that might confound the estimated relationship. Recently, the MiBioGen consortium [ 30 ] released numerous microbiome abundance-associated loci, offering an unprecedented chance to explore the causality between the gut microbiota and tobacco use. Based on the knowledge above, we hypothesized that the gut microbiome links smoking behaviors and conducted a two-sample bi-directional MR analysis to elucidate the causal association between the gut microbiota and smoking phenotypes and further explore the potential role of several metabolites on these associations.

An overview of the analytical plan is shown in Additional file 1 : Figure S1.

Data sources and instrumental variable selection

The data analyzed in this secondary study is publicly available from existing, published GWASs and therefore the ethical approval and informed consent have been obtained by all original studies (Table 1 ). Detailed information, such as recruitment criteria of population and quality control of genetic data, can be found in the original paper (Table 1 ). The source data and its related papers were found on PubMed and acquired easily on GWAS Catalog ( https://www.ebi.ac.uk/gwas/downloads/summary-statistics ). The search terms for summary statistics of gut microbes on PubMed was “gut microbiota” and “genome-wide association study”. The specific terms of smoking phenotypes and metabolites, for example smoking initiation or tryptophan, were directly used to found summary statistics on GWAS Catalog. These GWAS sample populations needed to be predominantly of European descent and largely independent of each other.

The genetic instrument variables (IVs), typically single-nucleotide polymorphisms (SNPs), for the gut microbiota were retrieved from a large-scale GWAS meta-analysis, which contained 18,340 European-dominated participants from 24 separate cohorts with 5,717,754 SNPs after imputation [ 31 , 32 ]. In the original study, the gut microbiota was categorized into 257 taxa at six taxonomic levels: phylum [p], class [c], order [o], family [f], and genus [g]. Of these, 211 taxa (9 phyla, 16 classes, 20 orders, 35 families, and 131 genera), which were eligible for the mbQTL (microbial quantitative trait locus) mapping analysis, were included in this study. The effect sizes of smoking-related SNPs were acquired from a meta-analyzed GWAS summary association data from 1,232,091 individuals with predominantly European ancestry [ 30 , 33 ], including age of smoking initiation (a continuous phenotype), smoking initiation (a binary phenotype, ever being a regular smoker), cigarettes per day (a continuous indicator of smoking heaviness), and smoking cessation (a binary phenotype, contrasting current versus former smokers). Of note, lifetime smoking was also included as a comprehensive phenotype, using data from the UK Biobank which recruited 462,690 European ancestry dominated samples [ 34 , 35 ]. The lifetime smoking is a continuous composite concept of the burden of lifetime exposure to smoking constructed by smoking initiation/cessation, smoking heaviness, and smoking duration.

Furthermore, we also sought to explore the potential role of neurotransmitters in the biological pathway of the microbiota to smoking. After a systematic literature search in PubMed (we only considered the metabolites whose serum levels were commonly measured in regular metabolomic studies), we identified several important neurotransmitter-associated metabolites (including tryptophan, tyrosine, phenylalanine, glutamate, glycine) that may closely relate to brain function, especially substance use disorder, which subsequently affect smoking [ 36 , 37 , 38 , 39 ]. In addition, we also considered an important group of bacterial metabolites (i.e., short-chain fatty acids). We extracted genetic data for these specific human blood metabolites (i.e., tryptophan, tyrosine, phenylalanine, glutamate, glycine, and valerate) from a GWAS comprising 7824 European adult individuals [ 40 , 41 ]. Specifically, tryptophan, tyrosine, phenylalanine, and glutamate are closely related to neurotransmitters, respectively, 5-HT, dopamine, endorphins, and GABA. Glycine itself is a kind of neurotransmitter [ 42 ]. Valerate belongs to the short-chain fatty acids, which could regulate the blood–brain barrier, myelin formation, vagal excitability, and microglia maturation [ 43 ].

The selection of IVs, the key to ensure the accuracy and robustness of the causal inferences, should meet MR’s three key assumptions (Fig. 1 ). Then, the following steps were performed. Firstly, palindromic variants with minor allele frequency greater than 0.4 were excluded; secondly, variants and their alleles were harmonized between the GWAS results of exposure and outcome; thirdly, independent SNPs (LD r 2 < 0.01 and clumping distance = 250 kb, based on the European-based 1000 Genome Projects reference panel) were selected at a compromised significant level (1 × 10 −6 ) due to the relatively small sample size for mbQTL identification. To mitigate the effect of weak IV bias, the regular genome-wide significance (5 × 10 −8 ) was retained as a sensitivity analysis.

Schematic representation of the a two-sample bi-directional Mendelian randomization analysis and b multivariable Mendelian randomization analysis. MR was used to evaluate the causal links between 211 microbial taxa and five smoking phenotypes with or without considering neurotransmitter-associated or bacterial metabolites. Three key assumptions of MR: (1) genetic variants must be associated with exposures, (2) genetic variants must not be associated with confounders, and (3) genetic variants must affect outcomes only through exposures, not through other pathways

The usage and interpretation of our MR study adhere to the STROBE-MR (Strengthening the Reporting of Observational Studies in Epidemiology-Mendelian Randomization) checklist [ 44 ] (Additional file 1 : Table S1) and the critical appraisal checklist proposed by Davies et al. [ 45 ] (Additional file 1 : Table S2).

Statistical analysis

The two-sample MR study was incorporated to evaluate the causal links between 211 microbial taxa and five smoking phenotypes. The list of covariates varies between original GWASs, but always included sex and age. The details can be found in the original studies. Causal effects were estimated by five high-efficiency methodologies: the multiplicative random-effects model for the inverse-variance weighted (IVW) method (as the main MR method) [ 46 ], a constrained maximum likelihood and model averaging-based MR method (cML-MA, also as the main MR method) [ 47 ], weighted median method (sensitivity analysis) [ 48 ], MR-Egger regression (sensitivity analysis) [ 49 ], and MR pleiotropy residual sum and outlier (MR-PRESSO) method (sensitivity analysis) [ 50 ]. Different approaches yield valid evidence under different assumptions. cML-MA, which without relying on the InSIDE assumption, was also applied as a complementary method in our study to control correlated and uncorrelated pleiotropic effects [ 47 ]. In addition, the Cochran’s Q test in IVW was adopted to test the heterogeneity among SNPs included in each analysis. The intercept from MR-Egger method was used to assess the Instrument Strength Independent of Direct Effect (InSIDE) assumption which assumes that the horizontal pleiotropic effects are independent of the variant-exposure associations. P intercept < 0.05 suggests the existence of horizontal pleiotropy. MR-PRESSO global test was also used to evaluate overall horizontal pleiotropy. Meanwhile, MR-PRESSO corrected for horizontal pleiotropy by outlier removal. The above series of analyses was repeated to explore the causality in the other way, i.e., the impacts of tobacco use on gut microbial composition. Finally, as an attempt to uncover possible vertical pleiotropic pathways that could arise from specific serum metabolites, the multivariable MR analyses including MVMR-IVW and MVMR-Egger were performed to estimate the causal effect of specific gut microbes on smoking after adjusting for six neurotransmitter-associated or bacterial metabolites simultaneously and separately. Parameter setting was the same as for univariate MR.

MR analyses were performed using the “TwoSampleMR” (version 0.5.6), “MRcML” (version 0.0.0.9), and “MendelianRandomization” (version 0.6.0) packages in R (version 4.1.2) [ 50 , 51 ]. The statistical significance of the MR effect estimate was defined as a false discovery rate (FDR) of < 10%, where the Benjamini–Hochberg procedure was used to correct for the number of taxa tested, accounting for multiple comparisons.

Causal effect of smoking on gut microbiota

To understand the consequences of smoking behaviors (including smoking initiation, cigarette per day, age of initiation, smoking cessation, and lifetime smoking) on the abundance of the gut microbiome, two-sample MR tests were performed. We tested the potential causality from smoking-related traits to all available gut taxa. Detailed significant results for the causal relationship from smoking phenotypes to gut microbial taxa are shown in Table 2 .

The results of IVW analyses showed that the genetic liability for smoking initiation had a causal contribution to an increased abundance of Intestinimonas[g] (Beta ± SE: 0.265 ± 0.090, P = 3.15e − 03), which was in line with the evidence from a mice model showing that exposure to the major cigarette smoke carcinogens (NNK plus BaP) could elevate fecal level of Intestinimonas [ 52 ] (Fig. 2 a). We also found that increased genetically predicted lifetime smoking was significantly related to higher abundance of Catenibacterium[g] (Beta ± SE: 0.505 ± 0.170, P = 2.98e − 03) as well as lower abundance of RuminococcaceaeNK4A214[g] (Beta ± SE: − 0.261 ± 0.074, P = 4.48e − 04) and RuminococcaceaeUCG005[g] (Beta ± SE: − 0.237 ± 0.076, P = 1.91e − 03), corroborating previous observational findings from two cross-sectional studies based on a Bangladeshi population [ 53 ] and a Chinese population [ 54 ], respectively (Fig. 2 b,c). The MR results also suggested that smoking initiation was causally associated with the abundance of Pasteurellales[o] (Beta ± SE: − 0.328 ± 0.097, P = 7.40e − 04), Pasteurellaceae[f] (Beta ± SE: − 0.328 ± 0.097, P = 7.40e − 04), Christensenellaceae[f] (Beta ± SE: − 0.278 ± 0.072, P = 1.18e − 04), ChristensenellaceaeR[g] (Beta ± SE: − 0.267 ± 0.073, P = 2.75e − 04), and Romboutsia[g] (Beta ± SE: − 0.279 ± 0.085, P = 1.06e − 03). A higher genetically predicted age of smoking initiation was causally related to a higher abundance of Lactococcus[g] (Beta ± SE: 1.135 ± 0.317, P = 3.45e − 04), but a lower abundance of Eisenbergiella[g] (Beta ± SE: − 1.062 ± 0.250, P = 2.21e − 05). Neither horizontal pleiotropy nor heterogeneity (among IVs) was detected at statistically significant levels (all P for Egger intercept > 0.05, most of the P for PRESSSO global test > 0.05, and all P for Cochran’s Q > 0.05). The results estimated by cML-MA method was highly consistent with the estimates using IVW. The FDR adjusted P -value and the family-wised corrected P -value could be found in Additional file 2 : Table S4.

The summary of the key findings in the univariable MR study . Combining with existing evidence, we consistently found the causal effect of smoking on a Intestinimonas , b Catenibacterium , c Ruminococcaceae , and provided novel insights regarding d the reward loop of smoking heaviness, e the influence of parental smoking on childhood smoking. Black solid arrows indicate known evidence, red solid arrows indicate what we found in this study, and red dashed arrow indicates potentially deducible conclusion

Causal effect of gut microbiota on smoking

The original GWAS involving 18,340 individuals from 24 cohorts provided summary statistics for 211 microbial taxa. Of them, 41 taxa providing greater than or equal to three IVs were included in this MR for testing the potential causal effect of the gut microbiome on smoking behaviors (40 taxa for lifetime smoking). Estimated by IVW test, six taxa were identified, after FDR correction, to reach a statistical significance. Concordant results were observed using cML-MA method (shown in Table 2 ).

The MR analysis revealed that the abundance of Actinobacteria[p] (Beta ± SE: − 0.066 ± 0.024, P = 5.31e − 03), Actinobacteria[c] (Beta ± SE: − 0.053 ± 0.018, P = 3.70e − 03), Bifidobacteriales[o] (Beta ± SE: − 0.048 ± 0.019, P = 1.12e − 02), Bifidobacteriaceae[f] (Beta ± SE: − 0.048 ± 0.019, P = 1.12e − 02), and Bifidobacterium[g] (Beta ± SE: − 0.048 ± 0.018, P = 8.83e − 03) were negatively associated with the number of cigarettes smoked per day. Increased abundance of Actinobacteria[p] (Beta ± SE: 0.051 ± 0.019, P = 7.74e − 03), Bifidobacteriales[o] (Beta ± SE: 0.050 ± 0.016, P = 1.73e − 03), Bifidobacteriaceae[f] (Beta ± SE: 0.050 ± 0.016, P = 1.73e − 03), and Bifidobacterium[g] (Beta ± SE: 0.049 ± 0.016, P = 1.79e − 03) lead to later smoking initiation. When considering lifetime smoking as an outcome, the results showed a trend similar to that of cigarettes per day analysis (detailed effect estimates are shown in Table 1 ). The sensitivity analyses did not show clear evidence of potential horizontal pleiotropy (all P for Egger intercept > 0.05, most of the P for PRESSSO global test > 0.05). Heterogeneity was not found among SNPs (all P for Cochran’s Q > 0.05).

Another two key findings are displayed in Fig. 2 d and e, indicating potential mechanisms of the gut-brain axis. All causal-effect estimates, including the sensitivity analyses, between 211 microbial taxa and five smoking phenotypes analyzed in this MR are presented in Additional file 2 : Table S4. All IVs used in our study are provided in Additional file 2 : Table S5. Additional visualizations of the results, including scatter plot, forest plot, and leave-one-out plot can be found in Additional file 1 : Figure S2-S5. Moreover, the MR results evaluated under two instrumental variable selection thresholds (1e − 6 vs. 5e − 8) were presented in Additional file 1 : Table S3, which indicated very limited difference on β -coefficients (Pearson r 1e-6v.s.5e-8 = 0.99, P < 0.001).

The effect of neurotransmitter-associated metabolites on observed associations

Considering the possible contribution of serum metabolites on the progress from the gut microbiota to smoking, we used multivariable MR for observed significant associations (the results in Table 2 ) with six neurotransmitter-associated or bacterial metabolites (tryptophan, tyrosine, phenylalanine, glutamate, glycine, and valerate) adjusted. The multivariable MR results are reported in Table 3 .

When adjusting the six metabolites together using MVMR-IVW, we found a noticeable increase in P -value for causal effect of Actinobacteria[c] ( P = 0.242) and Peptococcus[g] ( P = 0.502) on lifetime smoking, while the majority of results remained robust. Another change worth mentioning is that, by making rough comparisons, relatively lower β -coefficient (absolute value) for the associations between the gut microbiota and age of initiation were observed compared with the results without adjustment for the metabolites. Subsequently, focused on Actinobacteria[c] and Peptococcus[g] , we implemented adjustment of one metabolite at a time. Signals of decline in significance of association were detected for tryptophan ( P = 0.115 for Actinobacteria[g] ; P = 0.503 for Peptococcus[g] ), tyrosine ( P = 0.316 for Actinobacteria[g]; P = 0.558 for Peptococcus[g] ), and valerate ( P = 0.218 for Peptococcus[g] ). Additionally, the results of MVMR-Egger indicated that our multivariable MR estimates were unlikely biased by pleiotropy (most of P for MVMR-Egger intercept > 0.05).

The intriguing finding was presented in Fig. 3 , implying the role of metabolites in the action pathway from the gut microbiota to smoking.

The summary of the key findings in the multivariable MR study. Combining with existing evidence and biological mechanisms, we consistently found that tryptophan, tyrosine, and/or valerate may take part in the action pathways from a Peptococcus and b Actinobacteria to smoking. Black solid arrows indicate known evidence, black dashed arrows indicate biological hypothesis we introduced earlier, and red dashed arrow indicates potentially deducible conclusion. The bold dashed boxes are neurotransmitters that are closely related to corresponding metabolites and are likely involved in the mechanism by which smoking responds to the gut microbiota in a metabolite-dependent manner

To our best knowledge, this work is among the first to systematically evaluate the causal relationships between the gut microbiota and tobacco use from a genetic perspective. This two-sample MR study gave reasonably strong evidence that genetically predicted abundance of specific gut microbes play non-negligible roles in the occurrence and progression of cigarette smoking, in which, metabolites may be participating. As for the other direction, the MR confirmed and strengthened the role of smoking on the gut microbiota. Leveraging the power of molecular genetic markers as instrumental variables, the MR approaches largely avoided the interference of confounders (e.g., socioeconomic position, culture) and reversed causality which make regular observational study vulnerable [ 45 ].

As mentioned in the introduction, the theory of the microbiota-gut-brain communication hints at a possible influence of the gut microbiota on smoking. Nevertheless, few studies had directly explored this theme. Leveraging the large-scale GWAS data sources, our MR study filled this knowledge gap from a novel angle. (1) Previous studies indicated that smoking would decrease the abundance of Actinobacteria while our results found that a lower abundance of Actinobacteria may cause an increase in the number of cigarettes smoked per day, i.e., worse smoking status. More severe smoking conditions may in turn cause a further diminishment in Actinobacteria abundance, implying a potential positive feedback effect [ 10 , 55 ]. This might partially explain why smokers tend to increase the tobacco use. (2) In addition, observational research showed that, compared to infants from non-smoking families, those from smoking households had lower intestinal flora diversity and abundance, with Bifidobacterium in particular [ 56 ]. Interestingly, we found a lower abundance of Bifidobacterium may induce an earlier age of smoking initiation. While conventional wisdom has expounded that early smoking in children may result from early exposure to third-hand smoke or imitation of father’s smoking behavior [ 57 , 58 ], our study provides new insights that the early smoking initiation may be proportionally explained by gut flora. Regulating the gut microbiota, such as probiotic intervention, might be an option to redeem bad effects caused by premature smoke exposure.

Rather than just concerning the causality between the gut microbiota and smoking, we also considered the possible involvement of metabolites in this process. (1) Our results suggested an attenuated significance of association between Peptococcus and smoking after adjusting tryptophan and/or tyrosine, implying a potential metabolite-dependent mechanism of the microbiota on smoking that these two amino acids drove. Wen’s study, from another angle that using metabolomics and 16S rRNA gene sequencing analyses in the rat model, proved the correlation between Peptococcus and key metabolic pathways, also including tryptophan metabolism and tyrosine metabolism [ 59 ]. (2) MetOrigin is a bioinformatics tool, aiming to identify which bacteria and how they participate in certain metabolic reactions [ 60 ]. A similar implication in our multivariable MR analysis that tryptophan may modify the effects of Actinobacteria on smoking was also somewhat corroborated in this platform by a simple quick search, which supported the relationship between Actinobacteria and tryptophan synthase.

There is growing evidence, albeit some indirect, providing possible biological explanations for the mechanisms of commensal gut microbiota on smoking, particularly probiotics such as Bifidobacterium . (1) The vagus nerve is thought to be a major modulatory constitutive communication pathway between the intestinal bacteria and the brain. Bifidobacterium longum have been found, via the vagus nerve, to send signals to the brain, leading to the secretion of a higher level of dopamine [ 61 ]. Since dopamine is related to the brain's reward function, higher levels of dopamine will offset the euphoria of smoking or the pain of quitting, thereby reducing smoking addiction [ 62 ]. (2) Neurotransmitters probably mediate the influences of the intestinal microbiome on smoking. For instance, Bifidobacterium was reported to promote serotonin (5-HT) biosynthesis in colonic enterochromaffin cells by activating the CGA/ADRα2A cascade signal and regulating the TRP/TPH-OR pathways [ 63 , 64 ]. 5-HT has been the therapeutic target for addiction to alcohol, cocaine, or drug, so it may also be for smoking [ 65 ]. Other neurotransmitters with similar functions and previously shown to be influenced by Bifidobacterium also include GABA [ 66 ] and noradrenaline [ 67 ]. (3) The close link of metabolites (e.g., short-chain fatty acids [ 68 ], metabolite acetate [ 69 ]) or components (e.g., peptidoglycan [PGN]) of Bifidobacterium with the CNS may explain its effect on smoking. Short-chain fatty acids are relevant to the morphology and function of microglia [ 70 ], and metabolite acetate has therapeutic potential to prevent cognitive impairment [ 69 ]. PNG can penetrate the blood-brain barrier, entering the brain, and communicating with the PGN-sensing molecules (Pglyrp2) in the amygdala [ 71 , 72 ]. Accordingly, changes in metabolite levels resulting from gut flora dysbiosis make an unavoidable effect on CNS, releasing fear- or anxiety-like emotions or triggering depression, subsequently elevating the risk of smoking initiation or failure to smoking cessation [ 73 , 74 , 75 ]. The above biological evidence also explains, to some extent, why the relationship between the gut microbiota and smoking may be modified after adjusting for specific amino acids or short-chain fatty acids. A point worth noting is that these potential mechanisms are not fully evidenced. In addition, there is a non-negligible gap between nicotine cravings and the complex smoking behaviors/pattern observed at the population level. Future studies on the gut microbiome and smoking behaviors are anticipated. Certainly, before moving forward, specialized mechanistic investigations are needed to understand the distinct roles of individual taxa, as most of the currently available mechanistic explanations remain at the generalized whole-gut microbial level.

In the other direction, our findings strengthened and extended existing observational evidence, suggesting that tobacco smoking could disrupt the homeostasis of the intestinal microbiota. (1) Our study supported that initiation of smoking could increase Intestinimonas abundance, which showed consistency with the results obtained in a previous experimental study. Qu and colleagues observed an elevated level of Intestinimonas after exposure to NNK plus BaP in mice [ 52 ]. Notably, NNK and BaP, the products of smoking, are the major risk elements for inducing cellular carcinogenesis of lung cancer [ 76 ]. (2) The MR results confirmed the roles of smoking for a higher abundance of Catenibacterium and a lower abundance of Ruminococcaceae which were observed from two cross-sectional studies. In a Bangladeshi population, a study exhibited that the relative abundance of Catenibacterium was significantly higher in current smokers compared with never-smokers, showing a dose-response relationship with packs of cigarettes smoked per day [ 53 ]. Enrolling 116 healthy male subjects from China, an observational study revealed that smoking could lower the abundance of Ruminococcaceae , which was independent of BMI and age [ 54 ]. Importantly, MR design allows for more reliable results with the highest evidence hierarchy other than randomized controlled trials (RCT) [ 45 ]. (3) In addition, Wang et al. reported that cigarette smoking significantly reduced the level of Lactococcus [ 77 ]. The current MR study further pointed out that the younger the year of smoking initiation, the greater this reduction. (4) Apart from the above, there also appeared several significant evidence for the effect of smoking on Eisenbergiella , Pasteurellaceae , Christensenellaceae , Haemophilus , Romboutsia , and Coriobacteriaceae , which were rarely addressed or not clearly understood before. (5) Nevertheless, it was noteworthy that for some microbial taxa, such as Bifidobacterium and Actinobacteria , the existing literature reported the impact of smoking on these taxa, while our work did not provide corresponding strong causal evidence, although most of the effect estimates were consistent in the direction. The main mechanisms by which smoking affects the gut microbiota include the following: raising the pH of the intestinal environment [ 18 ], inducing chronic low-grade inflammation or inflammation-related diseases [ 78 ], as well as promoting oxidative stress [ 79 ].

Several limitations of our study should be acknowledged. Firstly, to reduce the potential effect of weak IV bias, we applied a stricter P -value cutoff (1e − 06), compared with 1e − 05 which was used in the original paper [ 31 ] and another recent paper [ 80 ]. Thus, it may result in insufficient statistical power, a critical reason for false negatives. Because of the large number of microbial taxa, as well as the hierarchical structure (the abundance could be highly correlated for a microbial strain), and correlations among smoking phenotypes, the multiple comparison adjustment, especially global multiple corrections, may be excessive, further affecting the false negative. Therefore, causality cannot be completely ruled out in negative results, which should be treated with caution. Secondly, since the majority of participants in the GWAS of tobacco use were ancestrally Europeans, extrapolation of the results in the present study to other ethnic groups might be limited. Thirdly, although most of the participants of the gut microbial GWAS were ancestrally Europeans, the ethnic proportion was not perfectly matched between the two samples (i.e., the exposure GWAS and the outcome GWAS dataset), which may result in some levels of inconsistency in LD correlations. Fourthly, smoking is predominantly prevalent among men, and the composition of the gut microbiota also somewhat varies by gender. However, our work cannot analyze the two genders separately. Likewise, the estimates of a lifetime effect of the gut microbiota on smoking provided by MR cannot deliver much clinical meaningful for age-specific interventions. The limited sample size may also prevent us from providing a sufficiently precise estimate as well as 95% confidence intervals for clinical practice. It would be helpful to perform a gender- or age-specific MR analysis especially with larger sample size in future endeavors. Finally, the metabolites analyzed in multivariable MR were detected in human serum. We think that more appropriate and direct information may be generated from fecal samples, but unfortunately, this kind of data is currently lacking. Additionally, direct analysis of all metabolites may leave the hypothesis without sufficient biological evidence, whereas a biologically informed selection may reduce significant findings. Of a certainty, there still exist other neurotransmitters such as norepinephrine as well as other more important short-chain fatty acids such as propionate and butyrate, but the summary data of itself or its related metabolites is also lacking.

Leveraging the publicly available genetic databases, bidirectional causal links between specific intestinal microbes and cigarette smoking were identified. Taking together the existing evidence, potential mechanisms including a positive feedback loop of smoking and the potential role of neurotransmitter-associated metabolic biomarkers therein were revealed. Our study highlighted the hazards of tobacco use for gut flora dysbiosis and shed light on the potential role of specific gut microbiota for tobacco use behaviors.

Availability of data and materials

The data used in this study is freely available for download in the MiBioGen repository, www.mibiogen.org , GSCAN repository, https://doi.org/10.13020/3b1n-ff32 , UK Biobank repository, https://doi.org/10.5523/bris.10i96zb8gm0j81yz0q6ztei23d , and the Metabolomics GWAS repository, http://metabolomics.helmholtz-muenchen.de/gwas , respectively.

Availability of code

The actual code used to run the analyses described in this study is available at the github site at https://github.com/zdangm/smoking_microbiome .

Abbreviations

5-Hydroxytryptamine, as known as serotonin

Benzo[a]pyrene

Body mass index

A constrained maximum likelihood and model averaging-based MR method

Central nervous system

False discovery rate

γ-Aminobutyric acid

Genome-wide association study

Instrument Strength Independent of Direct Effect

Instrument variable

Inverse-variance weighted

Linkage disequilibrium

Microbial quantitative trait locus

Mendelian randomization

MR pleiotropy residual sum and outlier

Multivariable Mendelian randomization

Nitrosamines 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone

PGN-sensing molecules

Peptidoglycan

Randomized controlled trial

Single-nucleotide polymorphism

W.H.O: Tobacco. [2022-07-28]. https://www.who.int/news-room/fact-sheets/detail/tobacco . Accessed 28 July 2022.

Vink JM, Boomsma DI. Interplay between heritability of smoking and environmental conditions? A comparison of two birth cohorts. BMC Public Health. 2011;11:316.

Article PubMed PubMed Central Google Scholar

Vink JM, Willemsen G, Boomsma DI. Heritability of smoking initiation and nicotine dependence. Behav Genet. 2005;35(4):397–406.

Article PubMed Google Scholar

Thursby E, Juge N. Introduction to the human gut microbiota. Biochem J. 2017;474(11):1823–36.

Article CAS PubMed Google Scholar

Valdes AM, Walter J, Segal E, Spector TD. Role of the gut microbiota in nutrition and health. BMJ. 2018;361: k2179.

Fan Y, Pedersen O. Gut microbiota in human metabolic health and disease. Nat Rev Microbiol. 2021;19(1):55–71.

Lynch SV, Pedersen O. The human intestinal microbiome in health and disease. N Engl J Med. 2016;375(24):2369–79.

Hasan N, Yang H. Factors affecting the composition of the gut microbiota, and its modulation. PeerJ. 2019;7: e7502.

Chang CS, Kao CY. Current understanding of the gut microbiota shaping mechanisms. J Biomed Sci. 2019;26(1):59.

Savin Z, Kivity S, Yonath H, Yehuda S. Smoking and the intestinal microbiome. Arch Microbiol. 2018;200(5):677–84.

Gui X, Yang Z, Li MD. Effect of cigarette smoke on gut microbiota: state of knowledge. Front Physiol. 2021;12: 673341.

Antinozzi M, Giffi M, Sini N, Galle F, Valeriani F, De Vito C, Liguori G, Romano Spica V, Cattaruzza MS. Cigarette smoking and human gut microbiota in healthy adults: a systematic review. Biomedicines. 2022;10(2):510.

Hu X, Fan Y, Li H, Zhou R, Zhao X, Sun Y, Zhang S. Impacts of cigarette smoking status on metabolomic and gut microbiota profile in male patients with coronary artery disease: a multi-omics study. Front Cardiovasc Med. 2021;8: 766739.

Article CAS PubMed PubMed Central Google Scholar

Yoon H, Lee DH, Lee JH, Kwon JE, Shin CM, Yang SJ, Park SH, Lee JH, Kang SW, Lee JS, et al. Characteristics of the gut microbiome of healthy young male soldiers in South Korea: the effects of smoking. Gut Liver. 2021;15(2):243–52.

Jung Y, Tagele SB, Son H, Ibal JC, Kerfahi D, Yun H, Lee B, Park CY, Kim ES, Kim SJ, et al. Modulation of gut microbiota in Korean navy trainees following a healthy lifestyle change. Microorganisms. 2020;8(9):1265.

Yang HT, Xiu WJ, Liu JK, Yang Y, Zhang YJ, Zheng YY, Wu TT, Hou XG, Wu CX, Ma YT, et al. Characteristics of the intestinal microorganisms in middle-aged and elderly patients: effects of smoking. ACS Omega. 2022;7(2):1628–38.

Ishaq HM, Shahzad M, Wu X, Ma C, Xu J. Molecular characterization of fecal microbiota of healthy Chinese tobacco smoker subjects in Shaanxi Province, Xi’an China. J Ayub Med Coll Abbottabad. 2017;29(1):3–7.

PubMed Google Scholar

Tomoda K, Kubo K, Asahara T, Andoh A, Nomoto K, Nishii Y, Yamamoto Y, Yoshikawa M, Kimura H. Cigarette smoke decreases organic acids levels and population of bifidobacterium in the caecum of rats. J Toxicol Sci. 2011;36(3):261–6.

Hu J, Wei T, Sun S, Zhao A, Xu C. Effects of cigarette smoke condensate on the production and characterization of exopolysaccharides by Bifidobacterium. An Acad Bras Cienc. 2015;87(2):997–1005.

Ridaura V, Belkaid Y. Gut microbiota: the link to your second brain. Cell. 2015;161(2):193–4.

Cryan JF, O’Riordan KJ, Cowan CSM, Sandhu KV, Bastiaanssen TFS, Boehme M, Codagnone MG, Cussotto S, Fulling C, Golubeva AV, et al. The microbiota-gut-brain axis. Physiol Rev. 2019;99(4):1877–2013.

Yang Z, Li J, Gui X, Shi X, Bao Z, Han H, Li MD. Updated review of research on the gut microbiota and their relation to depression in animals and human beings. Mol Psychiatry. 2020;25(11):2759–72.

Liu X, Tang S, Zhong H, Tong X, Jie Z, Ding Q, Wang D, Guo R, Xiao L, Xu X, et al. A genome-wide association study for gut metagenome in Chinese adults illuminates complex diseases. Cell Discov. 2021;7(1):9.

Spinella M. Correlations between orbitofrontal dysfunction and tobacco smoking. Addict Biol. 2002;7(4):381–4.

Hayashi T, Ko JH, Strafella AP, Dagher A. Dorsolateral prefrontal and orbitofrontal cortex interactions during self-control of cigarette craving. Proc Natl Acad Sci U S A. 2013;110(11):4422–7.

Meckel KR, Kiraly DD. A potential role for the gut microbiome in substance use disorders. Psychopharmacology. 2019;236(5):1513–30.

Kiraly DD, Walker DM, Calipari ES, Labonte B, Issler O, Pena CJ, Ribeiro EA, Russo SJ, Nestler EJ. Alterations of the host microbiome affect behavioral responses to cocaine. Sci Rep. 2016;6:35455.

Lee K, Vuong HE, Nusbaum DJ, Hsiao EY, Evans CJ, Taylor AMW. The gut microbiota mediates reward and sensory responses associated with regimen-selective morphine dependence. Neuropsychopharmacology. 2018;43(13):2606–14.

Chakrabarti A, Geurts L, Hoyles L, Iozzo P, Kraneveld AD, La Fata G, Miani M, Patterson E, Pot B, Shortt C, et al. The microbiota-gut-brain axis: pathways to better brain health. Perspectives on what we know, what we need to investigate and how to put knowledge into practice. Cell Mol Life Sci. 2022;79(2):80.

Liu M, Jiang Y, Wedow R, Li Y, Brazel DM, Chen F, Datta G, Davila-Velderrain J, McGuire D, Tian C, et al. Association studies of up to 1.2 million individuals yield new insights into the genetic etiology of tobacco and alcohol use. Nat Genet. 2019;51(2):237–44.

Kurilshikov A, Medina-Gomez C, Bacigalupe R, Radjabzadeh D, Wang J, Demirkan A, Le Roy CI, Raygoza Garay JA, Finnicum CT, Liu X, et al. Large-scale association analyses identify host factors influencing human gut microbiome composition. Nat Genet. 2021;53(2):156–65.

Kurilshikov A, Medina-Gomez C, Bacigalupe R, Radjabzadeh D, Wang J, Demirkan A, Le Roy CI, Raygoza Garay JA, Finnicum CT, Liu X et al : MiBioGen. 2021. www.mibiogen.org .

Liu M, Jiang Y, Wedow R, Li Y, Brazel DM, Chen F, Datta G, Davila-Velderrain J, McGuire D, Tian C et al : Data related to association studies of up to 1.2 million individuals yield new insights into the genetic etiology of tobacco and alcohol use. 2019. https://doi.org/10.13020/3b1n-ff32 .

Wootton RE, Richmond RC, Stuijfzand BG, Lawn RB, Sallis HM, Taylor GMJ, Hemani G, Jones HJ, Zammit S, Davey Smith G, et al. Evidence for causal effects of lifetime smoking on risk for depression and schizophrenia: a Mendelian randomisation study. Psychol Med. 2020;50(14):2435–43.

Richmond. R, Stujifzand. B, Lawn. R, Sallis. H, Taylor. G, Hemani. G, Jones. H, Zammit. S, Smith. GD: Genome-wide association study of lifetime smoking index in a sample of 462,690 individuals from the UK Biobank. 2019. https://doi.org/10.5523/bris.10i96zb8gm0j81yz0q6ztei23d .

Kondziella D. The top 5 neurotransmitters from a clinical neurologist’s perspective. Neurochem Res. 2017;42(6):1767–71.

Duman RS, Sanacora G, Krystal JH. Altered connectivity in depression: GABA and glutamate neurotransmitter deficits and reversal by novel treatments. Neuron. 2019;102(1):75–90.

Kaur H, Golovko S, Golovko MY, Singh S, Darland DC, Combs CK. Effects of Probiotic Supplementation on Short Chain Fatty Acids in the AppNL-G-F Mouse Model of Alzheimer’s Disease. J Alzheimers Dis. 2020;76(3):1083–102.

Fernstrom JD. Dietary precursors and brain neurotransmitter formation. Annu Rev Med. 1981;32:413–25.

Shin SY, Fauman EB, Petersen AK, Krumsiek J, Santos R, Huang J, Arnold M, Erte I, Forgetta V, Yang TP, et al. An atlas of genetic influences on human blood metabolites. Nat Genet. 2014;46(6):543–50.

Shin SY, Fauman EB, Petersen AK, Krumsiek J, Santos R, Huang J, Arnold M, Erte I, Forgetta V, Yang TP et al : An atlas of genetic influences on human blood metabolites. 2014. http://metabolomics.helmholtz-muenchen.de/gwas .

Tran SM, Mohajeri MH. The role of gut bacterial metabolites in brain development, aging and disease. Nutrients. 2021;13(3):732.

Dalile B, Van Oudenhove L, Vervliet B, Verbeke K. The role of short-chain fatty acids in microbiota-gut-brain communication. Nat Rev Gastroenterol Hepatol. 2019;16(8):461–78.

Skrivankova VW, Richmond RC, Woolf BAR, Davies NM, Swanson SA, VanderWeele TJ, Timpson NJ, Higgins JPT, Dimou N, Langenberg C, et al. Strengthening the reporting of observational studies in epidemiology using mendelian randomisation (STROBE-MR): explanation and elaboration. BMJ. 2021;375: n2233.

Davies NM, Holmes MV, Davey Smith G. Reading Mendelian randomisation studies: a guide, glossary, and checklist for clinicians. BMJ. 2018;362: k601.

Burgess S, Butterworth A, Thompson SG. Mendelian randomization analysis with multiple genetic variants using summarized data. Genet Epidemiol. 2013;37(7):658–65.

Xue H, Shen X, Pan W. Constrained maximum likelihood-based Mendelian randomization robust to both correlated and uncorrelated pleiotropic effects. Am J Hum Genet. 2021;108(7):1251–69.

Bowden J, Davey Smith G, Haycock PC, Burgess S. Consistent estimation in Mendelian randomization with some invalid instruments using a weighted median estimator. Genet Epidemiol. 2016;40(4):304–14.

Burgess S, Thompson SG. Interpreting findings from Mendelian randomization using the MR-Egger method. Eur J Epidemiol. 2017;32(5):377–89.

Verbanck M, Chen CY, Neale B, Do R. Detection of widespread horizontal pleiotropy in causal relationships inferred from Mendelian randomization between complex traits and diseases. Nat Genet. 2018;50(5):693–8.

Hemani G, Zheng J, Elsworth B, Wade KH, Haberland V, Baird D, Laurin C, Burgess S, Bowden J, Langdon R, et al. The MR-Base platform supports systematic causal inference across the human phenome. Elife. 2018;7:e34408.

Qu Z, Zhang L, Hou R, Ma X, Yu J, Zhang W, Zhuang C. Exposure to a mixture of cigarette smoke carcinogens disturbs gut microbiota and influences metabolic homeostasis in A/J mice. Chem Biol Interact. 2021;344: 109496.

Nolan-Kenney R, Wu F, Hu J, Yang L, Kelly D, Li H, Jasmine F, Kibriya MG, Parvez F, Shaheen I, et al. The association between smoking and gut microbiome in Bangladesh. Nicotine Tob Res. 2020;22(8):1339–46.

Lin R, Zhang Y, Chen L, Qi Y, He J, Hu M, Zhang Y, Fan L, Yang T, Wang L, et al. The effects of cigarettes and alcohol on intestinal microbiota in healthy men. J Microbiol. 2020;58(11):926–37.

Sublette MG, Cross TL, Korcarz CE, Hansen KM, Murga-Garrido SM, Hazen SL, Wang Z, Oguss MK, Rey FE, Stein JH. Effects of smoking and smoking cessation on the intestinal microbiota. J Clin Med. 2020;9(9):2963.

Northrup TF, Stotts AL, Suchting R, Matt GE, Quintana PJE, Khan AM, Green C, Klawans MR, Johnson M, Benowitz N, et al. Thirdhand smoke associations with the gut microbiomes of infants admitted to a neonatal intensive care unit: an observational study. Environ Res. 2021;197: 111180.

den Exter Blokland EA, Engels RC, Hale WW 3rd, Meeus W, Willemsen MC. Lifetime parental smoking history and cessation and early adolescent smoking behavior. Prev Med. 2004;38(3):359–68.

Article Google Scholar

Melchior M, Chastang JF, Mackinnon D, Galera C, Fombonne E. The intergenerational transmission of tobacco smoking–the role of parents’ long-term smoking trajectories. Drug Alcohol Depend. 2010;107(2–3):257–60.

Wen Z, He M, Peng C, Rao Y, Li J, Li Z, Du L, Li Y, Zhou M, Hui O, et al. Metabolomics and 16S rRNA gene sequencing analyses of changes in the intestinal flora and biomarkers induced by gastrodia-uncaria treatment in a rat model of chronic migraine. Front Pharmacol. 2019;10:1425.

Yu G, Xu C, Zhang D, Ju F, Ni Y. MetOrigin: Discriminating the origins of microbial metabolites for integrative analysis of the gut microbiome and metabolome. 2022;1(1):e10.

Bercik P, Park AJ, Sinclair D, Khoshdel A, Lu J, Huang X, Deng Y, Blennerhassett PA, Fahnestock M, Moine D, et al. The anxiolytic effect of Bifidobacterium longum NCC3001 involves vagal pathways for gut-brain communication. Neurogastroenterol Motil. 2011;23(12):1132–9.

Han W, Tellez LA, Perkins MH, Perez IO, Qu T, Ferreira J, Ferreira TL, Quinn D, Liu ZW, Gao XB, et al. A neural circuit for gut-induced reward. Cell. 2018;175(3):665-678 e623.

Tian P, Wang G, Zhao J, Zhang H, Chen W. Bifidobacterium with the role of 5-hydroxytryptophan synthesis regulation alleviates the symptom of depression and related microbiota dysbiosis. J Nutr Biochem. 2019;66:43–51.

Lu Y, Zhang Z, Tong L, Zhou X, Liang X, Yi H, Gong P, Liu T, Zhang L, Yang L, et al. Mechanisms underlying the promotion of 5-hydroxytryptamine secretion in enterochromaffin cells of constipation mice by Bifidobacterium and Lactobacillus. Neurogastroenterol Motil. 2021;33(7): e14082.

Kirby LG, Zeeb FD, Winstanley CA. Contributions of serotonin in addiction vulnerability. Neuropharmacology. 2011;61(3):421–32.

Duranti S, Ruiz L, Lugli GA, Tames H, Milani C, Mancabelli L, Mancino W, Longhi G, Carnevali L, Sgoifo A, et al. Bifidobacterium adolescentis as a key member of the human gut microbiota in the production of GABA. Sci Rep. 2020;10(1):14112.

Desbonnet L, Garrett L, Clarke G, Kiely B, Cryan JF, Dinan TG. Effects of the probiotic Bifidobacterium infantis in the maternal separation model of depression. Neuroscience. 2010;170(4):1179–88.

Cheng Y, Liu J, Ling Z. Short-chain fatty acids-producing probiotics: A novel source of psychobiotics. Crit Rev Food Sci Nutr. 2022;62(28):7929–59.

Kobayashi Y, Sugahara H, Shimada K, Mitsuyama E, Kuhara T, Yasuoka A, Kondo T, Abe K, Xiao JZ. Therapeutic potential of Bifidobacterium breve strain A1 for preventing cognitive impairment in Alzheimer’s disease. Sci Rep. 2017;7(1):13510.

Silva YP, Bernardi A, Frozza RL. The role of short-chain fatty acids from gut microbiota in gut-brain communication. Front Endocrinol (Lausanne). 2020;11:25.

Arentsen T, Khalid R, Qian Y, Diaz Heijtz R. Sex-dependent alterations in motor and anxiety-like behavior of aged bacterial peptidoglycan sensing molecule 2 knockout mice. Brain Behav Immun. 2018;67:345–54.

Arentsen T, Qian Y, Gkotzis S, Femenia T, Wang T, Udekwu K, Forssberg H, Diaz Heijtz R. The bacterial peptidoglycan-sensing molecule Pglyrp2 modulates brain development and behavior. Mol Psychiatry. 2017;22(2):257–66.

Langdon KJ, Bakhshaie J, Lopez A, Tavakoli N, Garey L, Raines AM, Kauffman BY, Schmidt NB, Zvolensky MJ. Anxiety sensitivity physical and cognitive concerns in relation to smoking-oriented cognition: an examination among treatment-seeking adults who smoke. J Addict Med. 2018;12(3):212–9.

Jia X, Gao Z, Hu H. Microglia in depression: current perspectives. Sci China Life Sci. 2021;64(6):911–25.

Prusakowski MK, Shofer FS, Rhodes KV, Mills AM. Effect of depression and psychosocial stressors on cessation self-efficacy in mothers who smoke. Matern Child Health J. 2011;15(5):620–6.

Kometani T, Yoshino I, Miura N, Okazaki H, Ohba T, Takenaka T, Shoji F, Yano T, Maehara Y. Benzo[a]pyrene promotes proliferation of human lung cancer cells by accelerating the epidermal growth factor receptor signaling pathway. Cancer Lett. 2009;278(1):27–33.

Wang H, Zhao JX, Hu N, Ren J, Du M, Zhu MJ. Side-stream smoking reduces intestinal inflammation and increases expression of tight junction proteins. World J Gastroenterol. 2012;18(18):2180–7.

Arnson Y, Shoenfeld Y, Amital H. Effects of tobacco smoke on immunity, inflammation and autoimmunity. J Autoimmun. 2010;34(3):J258-265.

Talukder MA, Johnson WM, Varadharaj S, Lian J, Kearns PN, El-Mahdy MA, Liu X, Zweier JL. Chronic cigarette smoking causes hypertension, increased oxidative stress, impaired NO bioavailability, endothelial dysfunction, and cardiac remodeling in mice. Am J Physiol Heart Circ Physiol. 2011;300(1):H388-396.

Liu X, Tong X, Zou Y, Lin X, Zhao H, Tian L, Jie Z, Wang Q, Zhang Z, Lu H, et al. Mendelian randomization analyses support causal relationships between blood metabolites and the gut microbiome. Nat Genet. 2022;54(1):52–61.

Download references

Acknowledgements

The data analyzed in this study was provided by MiBioGen consortium, GSCAN consortium, UK Biobank, and Shin’s Lab. We gratefully acknowledge their contributing studies and the participants in the corresponding studies without whom this effort would not be possible.

This work was supported by Fundamental Research Funds from the Central Universities of Zhejiang University and the National Natural Sciences Foundation of China (82204118).

Author information

Jiayao Fan and Yuan Zhou contributed equally.

Authors and Affiliations

School of Public Health and the Second Affiliated Hospital, Zhejiang University School of Medicine, 388 Yuhangtang Road, Hangzhou, 310058, China

Jiayao Fan, Ran Meng & Dan Zhou

Department of Epidemiology and Health Statistics, School of Public Health, Hangzhou Medical College, 481 Binwen Road, Hangzhou, 310053, China

Jiayao Fan, Jiahao Zhu & Yingjun Li

Department of Biostatistics and Center for Quantitative Sciences, Vanderbilt University Medical Center, Nashville, TN, USA

Department of Psychiatry, Sir Run-Run Shaw Hospital, School of Medicine, Zhejiang University, Hangzhou, China

Jinsong Tang

Division of Genetic Medicine, Department of Medicine, Vanderbilt University Medical Center, Nashville, TN, USA

Melinda C. Aldrich & Nancy J. Cox

Vanderbilt Genetics Institute, Vanderbilt University Medical Center, Nashville, TN, USA

Department of Epidemiology & Biostatistics, School of Public Health, Zhejiang University, 388 Yuhangtang Road, Hangzhou, 310058, Zhejiang, China

The Key Laboratory of Intelligent Preventive Medicine of Zhejiang Province, Hangzhou, Zhejiang, China

You can also search for this author in PubMed Google Scholar

Contributions

DZ, YJL, and YMZ were the major contributors in conceptualization. DZ, JYF, and YZ analyzed the data. RM, JST, JHZ, MCA, and NJC verified the correctness of the data. DZ, JYF, and YZ were major contributors in writing the manuscript. All authors read and approved the final manuscript.

Corresponding authors

Correspondence to Yimin Zhu , Yingjun Li or Dan Zhou .

Ethics declarations

Ethics approval and consent to participate.

This research has been conducted using published studies and consortia providing publicly available summary statistics. All original studies have been approved by the corresponding ethical review board, and the participants have provided informed consent. In addition, no individual-level data was used in this study. Therefore, no new ethical review board approval was required.

Consent for publication

Not applicable.

Competing interests

The authors declare that they have no competing interests.

Additional information

Publisher's note.

Springer Nature remains neutral with regard to jurisdictional claims in published maps and institutional affiliations.

Supplementary Information

Additional file 1: table s1..

Self-inspection results of STROBE-MR checklist of recommended items to address in reports of Mendelian randomization studies. Table S2. Self-inspection results of critical appraisal checklist proposed by Davies et al. for evaluating Mendelian randomization studies. Table S3. The MR results of causal links between gut microbiome and smoking phenotypes by using IVW method under two instrumental variable selection thresholds. Figure S1. Overview of the analytical plan and main findings. Figure S2. Scatter plot of associations between genetic variants and Actinobacteria[p] versus between genetic variants and Cigarettes Per Day. The slope of each line represents the causal effect estimate using the corresponding MR analysis model, and the intercept can be interpreted as an estimate of the average horizontal pleiotropic effect across the genetic variants. Figure S3. Forest plot of individual SNP estimates and summary estimates for the causal associations between Actinobacteria[p] abundance and Cigarettes Per Day. Figure S4. Leave-one-out plot to assess if a single SNP drives the causal association between Actinobacteria[p] abundance and Cigarettes Per Day. Figure S5. Funnel plot of MR estimation for the causal association between Actinobacteria[p] abundance and Cigarettes Per Day.

Additional file 2: Table S4.

All results of causal links between gut microbiome and smoking phenotypes. Table S5. Instrumental variables used in our study for univariate MR and multivariable MR, respectively.

Rights and permissions

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/ . The Creative Commons Public Domain Dedication waiver ( http://creativecommons.org/publicdomain/zero/1.0/ ) applies to the data made available in this article, unless otherwise stated in a credit line to the data.

Reprints and permissions

About this article

Cite this article.

Fan, J., Zhou, Y., Meng, R. et al. Cross-talks between gut microbiota and tobacco smoking: a two-sample Mendelian randomization study. BMC Med 21 , 163 (2023). https://doi.org/10.1186/s12916-023-02863-1

Download citation

Received : 19 November 2022

Accepted : 12 April 2023

Published : 28 April 2023

DOI : https://doi.org/10.1186/s12916-023-02863-1

Share this article

Anyone you share the following link with will be able to read this content:

Sorry, a shareable link is not currently available for this article.

Provided by the Springer Nature SharedIt content-sharing initiative

Gut microbiota
Tobacco smoking
Microbiota-gut-brain axis

BMC Medicine

ISSN: 1741-7015

Submission enquiries: [email protected]
General enquiries: [email protected]

IMAGES

Smoking Cessation Essay Example
📌 Essay Example on Smoking Cessation Program: A Public Health Success
SMOKING CESSATION _ CODP 8
Click to close or click and drag to move Essay Writing Examples, Best
Health Education Model For Smoking Cessation Essay Example
Smoking Cessation in Pregnancy

VIDEO

Smoking Cessation Counselling
The smoking essay // 10 line essay on smoking // Essay writing on smoking in English
Smoking Cessation
Smoking Cessation Interventions with Behavioral Health Populations
Smoking Essay in English 10 Lines || Short Essay on Smoking
Smoking Cessation: Past, Present, and Future

COMMENTS

Essay on Smoking in English for Students
500 Words Essay On Smoking. One of the most common problems we are facing in today's world which is killing people is smoking. A lot of people pick up this habit because of stress, personal issues and more. In fact, some even begin showing it off. When someone smokes a cigarette, they not only hurt themselves but everyone around them.
Tobacco Smoking and Its Dangers
Introduction. Tobacco use, including smoking, has become a universally recognized issue that endangers the health of the population of our entire planet through both active and second-hand smoking. Pro-tobacco arguments are next to non-existent, while its harm is well-documented and proven through past and contemporary studies (Jha et al., 2013).
Introduction, Conclusions, and the Evolving Landscape of Smoking Cessation
Tobacco smoking is the leading cause of preventable disease, disability, and death in the United States (U.S. Department of Health and Human Services [USDHHS] 2014). Smoking harms nearly every organ in the body and costs the United States billions of dollars in direct medical costs each year (USDHHS 2014). Although considerable progress has been made in reducing cigarette smoking since the ...
The hazards of smoking and the benefits of cessation: A critical
Smoking cessation benefits people at any age, but the benefits are greater at younger ages compared with older ages (Parish et al., 1995). The risk of coronary heart disease falls rapidly after cessation and then declines more slowly. The excess risk falls by about half after five years of cessation and then gradually approaches the risk of ...
235 Smoking Essay Topics & Titles for Smoking Essay + Examples
In your essay about smoking, you might want to focus on its causes and effects or discuss why smoking is a dangerous habit. Other options are to talk about smoking prevention or to concentrate on the reasons why it is so difficult to stop smoking. Here we've gathered a range of catchy titles for research papers about smoking together with ...
Essay on Stop Smoking
Despite the widespread knowledge of its harmful effects, many individuals continue to smoke, often due to addiction or social pressure. This essay aims to explore the reasons why it is crucial to stop smoking and the benefits that can be derived from it. The Health Hazards of Smoking. The primary reason to quit smoking revolves around health.
Effectiveness of stop smoking interventions among adults: protocol for
Smoking cessation can increase life expectancy by nearly a decade if achieved in the third or fourth decades of life. Various stop smoking interventions are available including pharmacotherapies, electronic cigarettes, behavioural support, and alternative therapies. This protocol outlines an evidence review which will evaluate the benefits and ...
Tobacco: Health benefits of smoking cessation
The Health Benefits of Smoking Cessation. U.S. Department of Health and Human Services, Public Health Service, Centers for Disease Control, Center for Chronic Disease Prevention and Health Promotion, Office on Smoking and Health. DHHS Publication No. (CDC) 90-8416. 1990. 4. Doll R, Peto R, Boreham J, Sutherland I. Mortality in relation to ...
Smoking: Effects, Reasons and Solutions
This damages the blood vessels. Smoking can result in stroke and heart attacks since it hinders blood flow, interrupting oxygen to various parts of the body, such as feet and hands. Introduction of cigarettes with low tar does not reduce these effects since smokers often prefer deeper puffs and hold the smoke in lungs for a long period.
Smoking Cessation: Guidance and Tips for Quitting
Chaiton M, Diemert L, Cohen JE, et al. Estimating the number of quit attempts it takes to quit smoking successfully in a longitudinal cohort of smokers. BMJ Open . 2016;6(6):e011045. doi:10.1136 ...
Smoking Cessation Essay
Smoking Cessation Essay. Smoking is a one of the major cause of increased mortality. More than 80% of smokers develop Chronic Obstructive Pulmonary Disease (COPD), making it one of the leading causes of death in the world (p.786). Smoking Cessation or quitting smoking is one of the most cost-effective ways to reduce the risk of COPD.
Smoking Cessation Strategies for the 21st Century
Smoking Cessation Strategies for the 21st Century. Cigarette smoking is the leading preventable cause of illness and premature death in the United States, claiming over 400 000 lives a year because it directly increases the risk of dying from heart disease, stroke, emphysema, and a variety of cancers. 1 Approximately 25% of adults in the United ...
Essay on Smoking Cessation Methods
Essay on Smoking Cessation Methods. Tobacco addiction contributes to approximately 438,000 deaths in the United States each year2, with smoking cigarettes constituting one of the most common preventable causes of death, on report asserts3. Tobacco use kills five million people a year worldwide, another source stresses4. Quitting smoking, or at ...
Smoking Cessation Interventions In England Health And Social Care Essay
The number of deaths attributed to smoking were estimated to be 83,900 in adults aged 35 and above in 2008. Among these deaths, 23,200 resulted from respiratory diseases (mainly obstructive lung disease) and 37,000 accounted for cancer conditions (lung cancer, Cancer of the Oesophagus). (HSCIC, 2009) Given the varied benefits of stopping ...
Examples & Tips for Writing a Persuasive Essay About Smoking
Persuasive Essay Examples About Smoking. Smoking is one of the leading causes of preventable death in the world. It leads to adverse health effects, including lung cancer, heart disease, and damage to the respiratory tract. However, the number of people who smoke cigarettes has been on the rise globally. A lot has been written on topics related ...
Reflective Essay on Smoking Cessation
Reflective Essay on Smoking Cessation. This essay provides a reflective account of the delivery of an opportunistic smoking cessation intervention. In constructing this account, Gibbs (1988) model of reflection has been utilised, which incorporates the following components: description; feelings; evaluation; analysis; conclusion; and action plan.
Behavioral Interventions Associated with Smoking Cessation in the
Brief advice/interventions. Brief advice on smoking cessation from a health care professional is effective in promoting cessation. This form of advice, particularly from general practitioners (GPs), leads 1 to 3 out of 100 smokers receiving it to stop smoking for at least 6 months.26 This is in addition to the number who would have stopped anyway.26 It is estimated that approximately 40% of ...
Smoking Cessation Essays (Examples)
Smoking Cessation Smoking is a central factor in many pathological conditions. Nearly all smokers have at least some idea of the risks associated with the practice yet chose to smoke anyway. The adverse effects of tobacco use on cardiopulmonary function are well established and recognized; less evident, but equally important, is its impact on all aspects of physical therapist practice ...
7 Common Withdrawal Symptoms
7. Feeling anxious, sad, or depressed. People who smoke are more likely to have anxiety or depression than people who don't smoke. Some people feel mood changes for a short time after they quit smoking. Watch for this, especially if you've ever had anxiety or depression.
Study finds methods to quit smoking effective regardless of mental
The most common smoking cessation aids were non-combustible nicotine products. Vaping products ( e-cigarettes) were used by 39% of people with a mental health condition and 31% of people without ...
Moderation of the real-world effectiveness of smoking cessation aids by
Objective To examine whether the real-world effectiveness of popular smoking cessation aids differs between users with and without a history of mental health conditions. Design Nationally-representative cross-sectional survey conducted monthly between 2016-17 and 2020-23. Setting England. Participants 5,593 adults (2,524 with a history of ≥1 mental health conditions and 3,069 without ...
Smoking Cessation and Patient Education in Nursing Essay
Smoking Cessation and Patient Education in Nursing Essay. A 50-year old male visited a nurse with a purpose of smoking cessation. While this process is considered complicated due to the smoking habit being a psychological trait, there are steps that should be followed for a successful outcome. Educating patients about smoking risks is an ...
Interventions for Smoking Cessation
The first step is to ask the client's smoking behavior and obtain the basic information about the client. Secondly, the readiness and motivation of clients to quit smoking will be assessed. In this step, stages of change model is a good tool to assess the motivation of client.
Smoking Cessation
Smoking cessation rates have been shown to increase from 12% in control groups to 28% in those using varenicline. In 2009, the FDA applied a black-box warning to varenicline because of safety reports of an association between the drug and adverse psychiatric events, including depressed mood, agitation, and suicidal behavior. ...
PDF Smoking Cessation after Transitioning from Hospital to Community Stop
4 . 1 However, in England t he available support outside hospital var ies depending on local resources 2 and policy. 13. Th.e main option for onwards support are community stop smoking services
Does e-cigarette use predict short-term smoking cessation behaviors
Among adults motivated to quit smoking, nicotine e-cigarette plus counseling vs counseling alone significantly increased point prevalence abstinence at 12 weeks, but the difference was no longer significant at 24 weeks, and trial interpretation is limited by early termination and inconsistent findings for nicotine and nonnicotine e-cigarettes ...
Nursing Interventions for Smoking Cessation Essay
This review is titled "Nursing Interventions for Smoking Cessation" and its main objective is to find out the effectiveness of nursing-initiated smoking cessation interventions (Rice, Hartmann‐Boyce & Stead, 2013). The review was mainly authored by Virginia Rice and Lindsay Stead and both authors are notable nursing authorities in the ...
Quit Connect Helps Black Patients with Rheumatoid Arthritis Quit Smoking
Each quit attempt cost approximately $4 to $10. Staff found the intervention feasible and acceptable. During two years in this safety-net rheumatology clinic serving predominantly Black patients, 58.9% of patients indicated readiness to cut back or quit smoking when asked. Post-implementation, among 550 visits with patients who smoked, 102 ...
1 Introduction, Summary, and Conclusions
Tobacco use is a global epidemic among young people. As with adults, it poses a serious health threat to youth and young adults in the United States and has significant implications for this nation's public and economic health in the future (Perry et al. 1994; Kessler 1995). The impact of cigarette smoking and other tobacco use on chronic disease, which accounts for 75% of American spending ...
Cross-talks between gut microbiota and tobacco smoking: a two-sample
Considerable evidence has been reported that tobacco use could cause alterations in gut microbiota composition. The microbiota-gut-brain axis also in turn hinted at a possible contribution of the gut microbiota to smoking. However, population-level studies with a higher evidence level for causality are lacking. This study utilized the summary-level data of respective genome-wide association ...