cause and effect model essay

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Mastering the art of writing a cause and effect essay – a comprehensive guide for students.

Have you ever wondered about the intricate web of causes and effects that shape our daily lives? The world is an interconnected tapestry, where actions lead to consequences and ripple effects can be felt far and wide. Delving into the realm of cause and effect essay writing allows us to explore this fascinating phenomenon and shed light on the intricate dynamics that drive our world.

Unlocking the secrets of causality becomes a thrilling adventure, where we unravel the threads that bind seemingly unrelated events. This form of essay is a powerful tool to analyze the core reasons behind certain outcomes and elucidate the multifaceted consequences that follow. As we embark on this journey, we will discover that cause and effect essay writing is not merely an exercise in academic observation, but a transformative process that enhances our analytical skills and deepens our understanding of the world.

Embracing the challenge of writing a cause and effect essay grants us the opportunity to gain mastery over the art of logical reasoning and critical thinking. Through meticulous examination and careful evaluation, we can trace the roots of various phenomena, untangle the intricacies of cause and effect relationships, and unlock a deeper comprehension of our surroundings.

Choosing a Topic for Your Cause and Effect Essay

When it comes to crafting a compelling cause and effect essay, one of the most vital steps is selecting the right topic. The topic you choose will lay the groundwork for the entire essay, determining the direction and scope of your analysis. It is essential to choose a topic that is not only engaging but also allows for a deeper exploration of the cause and effect relationship.

To begin, consider your personal interests and passions. Reflect on the issues or phenomena that have caught your attention and inspired your curiosity. By selecting a topic that genuinely interests you, you will be more motivated to dive into thorough research and analysis, resulting in a more compelling essay.

In addition to personal interests, it is also crucial to consider the current relevance and significance of a topic. Look for subjects that are currently generating discourse or have real-life implications. Choosing a topic that is timely and meaningful will not only enhance the relevance of your essay but also demonstrate your understanding of the broader context.

Furthermore, consider the available resources for research. Ensure that there is ample information and scholarly resources available on the topic you choose. Adequate research material will allow for a comprehensive understanding of the cause and effect relationship, enabling you to provide well-supported arguments in your essay.

Lastly, it is important to select a topic that is neither too broad nor too narrow. A broad topic may result in a superficial analysis, while a narrow topic may restrict your ability to explore the cause and effect relationship fully. Striking the right balance will ensure that you can provide a comprehensive analysis within the scope of your essay.

By considering your personal interests, the current relevance of a topic, the availability of research material, and the scope of analysis, you can choose a topic that will lay the foundation for an engaging and insightful cause and effect essay.

Discover how to select a captivating topic that will captivate your audience

When it comes to writing a compelling cause and effect essay, one of the most important factors is choosing a captivating topic that will engage and capture the interest of your readers. The topic you select sets the stage for the entire essay, determining the tone, focus, and overall impact of your writing.

It is crucial to choose a subject that is not only interesting but also relevant and meaningful. Selecting a topic that resonates with your readers will not only motivate them to continue reading but also to connect with and appreciate the content you are presenting.

Consider selecting a topic that is current and trending, as this will immediately grab the attention of your audience. You can explore current events, social issues, or even pop culture phenomena that have a cause and effect relationship worth examining. By choosing a topic that is relevant to the lives of your readers, you are more likely to capture their interest and make them invested in your essay.

Another approach to selecting a compelling topic is to target a subject that is controversial or thought-provoking. Controversial topics often spark debates and discussions, which can create a sense of excitement and engagement among your readers. By presenting different perspectives and analyzing the cause and effect relationships of a controversial issue, you can encourage your audience to think critically and consider different viewpoints.

Additionally, selecting a topic that is unique and rarely explored can also be an effective way to engage your readers. By presenting them with fresh and interesting content, you can pique their curiosity and keep them hooked throughout your essay. Look for lesser-known cause and effect relationships or delve into a subject that hasn’t been extensively covered to provide your readers with a unique and captivating reading experience.

In conclusion, choosing a compelling topic for your cause and effect essay is essential in capturing the attention and interest of your readers. By selecting a relevant, controversial, or unique subject, you can pique their curiosity and make them invested in your writing. Remember to consider your audience’s interests and values when choosing a topic to ensure that it resonates with them and keeps them engaged from start to finish.

Learn the essential components and organization of this type of academic writing

Understanding how to write a cause and effect essay involves knowing the key elements and structure that make up this particular type of academic writing. By grasping the essential components and organization, you will be equipped to effectively convey the relationship between causes and effects in your essay.

One important component of a cause and effect essay is the introduction, which provides an overview of the topic and clearly states the thesis statement. The thesis statement should express the main idea or argument of the essay, outlining the causes and effects that will be discussed.

Following the introduction, the body paragraphs of the essay delve into specific causes and effects. Each paragraph should focus on a single cause or effect, providing clear explanations and supporting evidence. It is important to use transitional words and phrases to guide the reader through the essay, making connections between causes and effects.

Additionally, proper organization is key in a cause and effect essay. One common approach is the chronological organization, where causes are presented in the order in which they occurred, leading to the effects. Another approach is the categorical organization, where causes and effects are grouped together based on common themes or categories.

Finally, a cause and effect essay should conclude with a clear summary of the main points and a restatement of the thesis statement. The conclusion should leave a lasting impression on the reader, emphasizing the significance of the causes and effects discussed in the essay.

By understanding and implementing the essential components and organization of a cause and effect essay, you can effectively analyze and present the causal relationships between events or phenomena. This type of academic writing allows you to explore the causes and effects of various topics, providing a deeper understanding and insight into the subject matter.

Gathering Evidence for Your Cause and Effect Analysis

When it comes to crafting a compelling cause and effect analysis, gathering solid evidence is crucial. In order to effectively support your claims and establish the cause-effect relationship, it is important to gather relevant and reliable evidence from various sources. By doing so, you can strengthen your arguments and provide a well-rounded understanding of the topic at hand.

Identify the Cause and Effect

Before you begin gathering evidence, it is necessary to clearly identify the cause and effect you will be exploring in your essay. This will help you focus your research and ensure that the evidence you collect directly supports your analysis. Clearly defining the cause and effect will also assist you in avoiding any potential tangents or unrelated information in your essay.

Research Scholarly Sources

A key element in gathering evidence for your cause and effect essay is conducting thorough research using reputable, scholarly sources. These sources can include academic journals, books, government publications, and authoritative websites. By utilizing these resources, you will be able to access well-researched and reliable information that adds credibility to your analysis.

Interview Experts or Professionals

In addition to scholarly sources, interviewing experts or professionals in the field related to your cause and effect topic can provide valuable insights and firsthand knowledge. These individuals can offer unique perspectives and experiences that can enhance the depth and quality of your analysis. Be sure to prepare thoughtful and relevant questions to make the most out of your interviews.

Gather Statistical Data

Statistics play a crucial role in a cause and effect essay as they provide quantifiable evidence to support your claims. Gathering statistical data, such as surveys, studies, or reports, helps to strengthen the cause-effect relationship by presenting concrete numbers and trends. Ensure that the statistical data you use is reliable and from credible sources in order to maintain the integrity of your analysis.

Utilize Case Studies or Examples

Using case studies or examples can further enhance the evidence used in your cause and effect analysis. Real-life examples or specific cases provide a practical understanding of the cause-effect relationship and make it easier for readers to connect with your arguments. Choose case studies or examples that are relevant to your topic and effectively illustrate the cause and effect you are discussing.

Gathering evidence is an essential step in writing a compelling cause and effect analysis. By clearly identifying the cause and effect, conducting thorough research, interviewing experts, utilizing statistical data, and incorporating case studies or examples, you can effectively support your claims and provide a well-rounded analysis. Remember to use reliable sources and present the evidence in a clear and organized manner to strengthen your arguments and engage your readers.

Explore effective research methods to support your claims and strengthen your arguments

In order to write a compelling cause and effect essay, it is crucial to support your claims and strengthen your arguments with solid research. By utilizing effective research methods, you can gather relevant evidence and data to back up your statements and make your essay more convincing. This section will explore various research techniques that can help you in this process.

One effective research method is conducting interviews. By directly speaking with experts or people with firsthand experience on the topic you’re discussing, you can gather valuable insights and personal anecdotes that can enrich your writing. Interviewing individuals who have a deep understanding of the cause-and-effect relationship you’re exploring can provide unique perspectives and strengthen your arguments.

Another research method to consider is conducting surveys or questionnaires. By designing well-crafted questions and distributing them to a relevant sample group, you can collect quantitative data that supports your claims. Surveys allow you to gather a large amount of information efficiently and objectively. This data can then be used to analyze patterns, trends, and correlations, which can further strengthen your arguments.

Utilizing scholarly sources such as academic journals and books is also an effective research approach. These sources provide in-depth analysis, research findings, and scholarly opinions on the causes and effects you’re discussing. By referencing reputable and authoritative sources, you can lend credibility to your arguments and demonstrate that your claims are well-supported by existing literature in the field.

Additionally, incorporating statistical data and empirical evidence can significantly strengthen your reasoning. By citing statistics, figures, and studies that provide concrete evidence of the cause-and-effect relationship you’re exploring, you can make your arguments more persuasive. This kind of data adds an objective and factual element to your essay, making it more compelling to readers.

By exploring and utilizing these research methods, you can ensure that your cause and effect essay is well-supported and thoroughly grounded in evidence. The combination of qualitative and quantitative data, expert insights, and scholarly sources will strengthen your arguments and make your essay more persuasive and credible.

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10.8 Cause and Effect

Learning objectives.

• Determine the purpose and structure of cause and effect in writing.
• Understand how to write a cause-and-effect essay.

The Purpose of Cause and Effect in Writing

It is often considered human nature to ask, “why?” and “how?” We want to know how our child got sick so we can better prevent it from happening in the future, or why our colleague a pay raise because we want one as well. We want to know how much money we will save over the long term if we buy a hybrid car. These examples identify only a few of the relationships we think about in our lives, but each shows the importance of understanding cause and effect.

A cause is something that produces an event or condition; an effect is what results from an event or condition. The purpose of the cause-and-effect essay is to determine how various phenomena relate in terms of origins and results. Sometimes the connection between cause and effect is clear, but often determining the exact relationship between the two is very difficult. For example, the following effects of a cold may be easily identifiable: a sore throat, runny nose, and a cough. But determining the cause of the sickness can be far more difficult. A number of causes are possible, and to complicate matters, these possible causes could have combined to cause the sickness. That is, more than one cause may be responsible for any given effect. Therefore, cause-and-effect discussions are often complicated and frequently lead to debates and arguments.

Use the complex nature of cause and effect to your advantage. Often it is not necessary, or even possible, to find the exact cause of an event or to name the exact effect. So, when formulating a thesis, you can claim one of a number of causes or effects to be the primary, or main, cause or effect. As soon as you claim that one cause or one effect is more crucial than the others, you have developed a thesis.

Consider the causes and effects in the following thesis statements. List a cause and effect for each one on your own sheet of paper.

• The growing childhood obesity epidemic is a result of technology.
• Much of the wildlife is dying because of the oil spill.
• The town continued programs that it could no longer afford, so it went bankrupt.
• More young people became politically active as use of the Internet spread throughout society.
• While many experts believed the rise in violence was due to the poor economy, it was really due to the summer-long heat wave.

Write three cause-and-effect thesis statements of your own for each of the following five broad topics.

• Health and nutrition

The Structure of a Cause-and-Effect Essay

The cause-and-effect essay opens with a general introduction to the topic, which then leads to a thesis that states the main cause, main effect, or various causes and effects of a condition or event.

The cause-and-effect essay can be organized in one of the following two primary ways:

• Start with the cause and then talk about the effects.
• Start with the effect and then talk about the causes.

For example, if your essay were on childhood obesity, you could start by talking about the effect of childhood obesity and then discuss the cause or you could start the same essay by talking about the cause of childhood obesity and then move to the effect.

Regardless of which structure you choose, be sure to explain each element of the essay fully and completely. Explaining complex relationships requires the full use of evidence, such as scientific studies, expert testimony, statistics, and anecdotes.

Because cause-and-effect essays determine how phenomena are linked, they make frequent use of certain words and phrases that denote such linkage. See Table 10.4 “Phrases of Causation” for examples of such terms.

Table 10.4 Phrases of Causation

The conclusion should wrap up the discussion and reinforce the thesis, leaving the reader with a clear understanding of the relationship that was analyzed.

Be careful of resorting to empty speculation. In writing, speculation amounts to unsubstantiated guessing. Writers are particularly prone to such trappings in cause-and-effect arguments due to the complex nature of finding links between phenomena. Be sure to have clear evidence to support the claims that you make.

Look at some of the cause-and-effect relationships from Note 10.83 “Exercise 2” . Outline the links you listed. Outline one using a cause-then-effect structure. Outline the other using the effect-then-cause structure.

Writing a Cause-and-Effect Essay

Choose an event or condition that you think has an interesting cause-and-effect relationship. Introduce your topic in an engaging way. End your introduction with a thesis that states the main cause, the main effect, or both.

Organize your essay by starting with either the cause-then-effect structure or the effect-then-cause structure. Within each section, you should clearly explain and support the causes and effects using a full range of evidence. If you are writing about multiple causes or multiple effects, you may choose to sequence either in terms of order of importance. In other words, order the causes from least to most important (or vice versa), or order the effects from least important to most important (or vice versa).

Use the phrases of causation when trying to forge connections between various events or conditions. This will help organize your ideas and orient the reader. End your essay with a conclusion that summarizes your main points and reinforces your thesis. See Chapter 15 “Readings: Examples of Essays” to read a sample cause-and-effect essay.

Choose one of the ideas you outlined in Note 10.85 “Exercise 3” and write a full cause-and-effect essay. Be sure to include an engaging introduction, a clear thesis, strong evidence and examples, and a thoughtful conclusion.

Key Takeaways

• The purpose of the cause-and-effect essay is to determine how various phenomena are related.
• The thesis states what the writer sees as the main cause, main effect, or various causes and effects of a condition or event.

The cause-and-effect essay can be organized in one of these two primary ways:

• Start with the cause and then talk about the effect.
• Start with the effect and then talk about the cause.
• Strong evidence is particularly important in the cause-and-effect essay due to the complexity of determining connections between phenomena.
• Phrases of causation are helpful in signaling links between various elements in the essay.

Writing for Success Copyright © 2015 by University of Minnesota is licensed under a Creative Commons Attribution-NonCommercial-ShareAlike 4.0 International License , except where otherwise noted.

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• Ultimate Guide to Craft Compelling Cause and Effect Essay
• Mastering The Art of Academic Essay Writing With Examples

Cause and effect essays are among the most usual essay types that students get to write at college. While the initial idea of writing a cause and effect essay may seem pretty simple, all you need to do is list the causes of a problem followed by the solutions. However, it is much easier said than done because essentially cause and effect essays are slightly tricky and require enormous brainstorming.

Table of Contents

• What is a cause and effect essay
• How to structure the cause and effect essay
• Hook of a cause and effect essay
• Background brief of a cause and effect essay
• Thesis statement of a cause and effect essay
• Outline of a cause and effect essay
• Body of a cause and effect essay
• Conclusion of a cause and effect essay

Besides the research you put in, the format of a cause and effect essay is as important. You need to ensure that you are presenting the essay in a standardized format to meet your academic goals and fetch some extra credits. Now the question is, what is a standardized format for writing a cause and effect essay? Well, this is your complete guide to cause and effect essays explaining each step in detail along with examples. So, let us get started.

What is a cause and effect essay?

A cause-and-effect essay is a type of expository essay that focuses on identifying the various causes and effects of a topic (problem) and explaining the detailed relationships between them. This type of academic writing basically focuses on the relationship between the causes (reasons) and effects (results) of a problematic scenario or trend. This is the reason, it is also called the reasons and results essay.

These types of essays are meant to explain why it happened and how it happened. For a better understanding of the concept, let’s have a look at some of the examples of what possibly could be the topics for different cause and effect essays.

• Discuss the various causes and effects of global warming on the earth.
• Elaborate on the different causes and effects of air pollution on the environment.
• Shed light on the causes and effects of social media addiction.

Now from the above examples, you got a clear idea of what exactly cause and effect essays look like. Hence, it is now time to understand the structure of writing a good cause and effect essay. That being the case, the next section will shed light on the structure of writing an impressive cause and effect essay.

How to structure the cause and effect essay?

The right structure of an essay is a key element that leads to writing an impressive essay. In the context of a cause and effect essay, the structuring is even more important because it allows your readers to clearly understand and easily navigate through the main ideas of your essay. Besides, right structuring also accounts for scores in essay writing. Hence, it is really essential to structure your essay in an effective way. To continue, like every other essay, the structure of the cause and effect essay also contains three main sections;

• Introduction
• Body paragraphs

However, the difference lies between the ideas and opinions you present in the essay and the way you present them in the essay. Hence, the further sections will effectively guide on how to write an introduction , thesis statement, outline, body paragraphs, and conclusion of a cause and effect essay. So, let’s move ahead further and start with the introduction of an essay.

How to write the introduction of a cause and effect essay?

Be it in essays, journals, articles, or research papers, the introduction of any form of writing is its make or break point. Hence, it is essential to grab the readers' attention right from the beginning. To elaborate, in the introduction, you will introduce the bigger circle of your essay i.e. the main topic of the essay which will assist your readers in understanding the context and the purpose of your essay writing. In the context of a cause and effect essay, the introduction will introduce the readers to the main topic first before moving ahead in explaining the different causes and effects and their correlation to the main topic.

For example, let’s say you are writing about the cause and effects of global warming. In the introduction, you will introduce your readers to the concept of global warming in detail before heading to its cause and effect. This introduction will assist your readers in comprehending the main reason why the essay topic needs to be discussed. However, in the introduction as well, there are 5 major aspects that need to be discussed.

• Background information
• Thesis statement

The further section will deliberately explain how to write all the 5 elements that will assist you in writing an essay. Besides, in the context of a cause and effect essay, the same example describing each element will be provided for your better understanding.

Introduction element: Hook of a cause and effect essay

A hook is a surprising element that engages your audience in your essay right from its beginning. Talking contextually, in a cause and effect essay, the hook can be statistical data or a claim that will clearly reflect the urgency of the discussion of your chosen topic. Let’s have a look at the sample hook in our taken example topic.

Sample hook

By the end of 2022, the temperature of the earth’s surface was around 0.98 Celsius degrees warmer than the average of the 20th century. Besides, the current global temperature has been consistently high on record("Topic: Global climate change", 2022).

In this hook, you might have noticed that we have given statistical data that directly points toward global warming. This will engage the readers right away and will encourage them to go through your essay till the end. Next, comes the background information.

Introduction element: Background brief of a cause and effect essay

Background information is necessary for an essay to brief the readers about the concept that will be discussed throughout the essay. In the case of a cause and effect essay, providing background information is even more important because the cause and effect of a topic will only be impactful when your readers would have good knowledge about the topic.

Let’s look at the background brief in the case of our sample essay topic for a better understanding of the background brief.

Sample Background Information

Global warming has been a concerning issue for a long time now. It has various effects on the environment that needs the attention of today’s generation. The number of cyclones, droughts, floods, and other natural disasters is increasing at a rampant pace. Besides, the main cause behind all these natural disasters is global warming.

After effectively providing the background information, using 2 to 3 lines, you will explain the purpose of writing an essay. This will allow you to draw the importance of the topic in the minds of the reader. To explain, you will answer the question, “Why is this topic important?”. After defining the purpose the next paragraph of your essay will talk about the thesis statement.

Introduction element: The thesis statement of a cause and effect essay

A thesis statement defines the topic in a summary that will be discussed in the essay. In terms of the cause and effect essay, in the thesis statement, you can narrow down the topic and let your audience know that this essay will provide different causes and effects briefly. Although every essay has a different thesis statement, the thesis statement of the cause and effect essay should follow the 3Cs formula explained below.

• Contentious: It is essential to know that your thesis statement should never contain any obvious facts. It should be contentious enough to intrigue the minds of readers and keep them indulged in the essay.
• Concise: The thesis statement of your essay should be concise so that your readers get a clear understanding of the central idea of the topic whose causes and effects would be discussed in the whole essay.
• Coherent: Lastly, there should be cohesion between your thesis statement and your body paragraphs describing different causes and effects of the essay.

In terms of our example, below given will be the thesis statement of your essay.

Sample thesis

Global warming can be understood as a direct consequence of various primary and secondary causes which could be either natural or man-made. Subsequently, the consequences of global warming can be quite detrimental to the planet and could result in some alarming effects.

If you want to learn more about thesis statements, you can go through our comprehensive guide on how to write a thesis statement .

Introduction element: Outline of a cause and effect essay

An outline is one of the most vital parts of the essay as it acts as the road map of your essay. To elaborate, the outline of an essay will briefly define all the aspects that your essay will cover and in what sequence of paragraphs it will be covered.

The outline of the essay allows the readers to understand how different cause-and-effect relationships will take place in the essay. Moreover, it will also allow you to survey and analyze the information before presenting it to your audience.

While writing an outline of the essay, you should note that your outline statement should clearly highlight the different cause and effect aspects that you will discuss in your essay.

Sample Outline

Firstly, the essay will talk about the main causes that are increasing the temperature all over the globe. Secondly, the effects that are caused by global warming will be discussed in the essay. Lastly, some of the solutions that will assist in dealing with the rising temperature of the earth will be provided in the essay.

How to write the body of a cause and effect essay?

There are two types of ways in which you can structure the body paragraph of your cause and effect essay i.e. block method and the chain method. In the block method, the writer first explains all the causes in the initial paragraphs and then explains the effect of each cause followed by a transition paragraph that will form the cohesion. Whereas, in the chain method, each cause is followed by its effect immediately.

To elaborate, each body paragraph of the cause and effect essay will start with a topic sentence that can either describe the main idea of the cause or the effect that will be discussed in the rest of the essay. After that, you will explain the topic sentence which can be a cause or the effect with the evidence (if possible) to support your topic sentence.

Moreover, if you do not have evidence, you will critically analyze and explain how your causes or effects fit in the bigger picture of your chosen topic of the subject. Lastly, the body paragraph will contain a cohesion line that will form a connection between the current paragraph and the beginning of the next paragraph.

In the case of our example, we will use the chain method and our body paragraph would be like this:

Sample Body Paragraph

There are different causes of global warming for which mankind is responsible. Deforestation is the major cause of rising global warming on the earth because plants are a major source of oxygen for all living organisms on the earth. Besides, they consume carbon dioxide which assists in maintaining the balance of the earth and evening things out. However, humans are recklessly cutting trees which have to lead to an imbalance in the environment. 13 million hectares of forest have been cut down and are converted for other uses(Deforestation Facts and Statistics,2022). This environmental imbalance is causing a rise in the temperature thus enhancing global warming. Not only this, there are many natural causes of global warming as well.

How to write the conclusion of a cause and effect essay?

The essay's conclusion should always consist of restating the main idea of causes and effects discussed in the whole essay. However, a notable fact while writing a conclusion is that you should never provide new information whether factual or literary in the conclusion paragraph.

You eventually have to present the thesis statement once again with the central idea around which your cause and effect essay revolved throughout. Along with this, you can also provide future implications directed toward tackling the effects of the different causes discussed in the essay. In the case of our example, the conclusion would be:

Sample Conclusion

To conclude, global warming is a concerning issue and the rising temperature is an alarm that needs our utmost attention right now. Hence, it is essential to know about the various causes of global warming and the impacts that it is bringing to the earth. So that we can take effective solutions to counter the situation in an effective manner.

To conclude, we are sure that the above guide has cleared all your doubts about the cause and effect essay. So, what are you waiting for? Use effective guidance and share it with your friends as well. So, you pass with flying colors and with HD grades in your assessments.

Recommended Readings

How to Write an Argumentative Essay

How to Write a Narrative Essay

What is the basic rule of cause and effect essay?

Cause and effect essays follow a simple rule of beginning with a topic sentence and then it’s followed by supporting details. Just assume, that your topic sentence talks about an effect, then the supporting details will describe its causes.

Can I use personal experiences in a cause and effect essay?

Yes, incorporating personal experiences can add depth and authenticity to your essay, especially when illustrating the effects of specific causes. However, ensure that your personal anecdotes support the main thesis and contribute to the overall understanding of the topic.

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Cause And Effect Essay Writing

How to Write Cause and Effect Essays in Simple Steps

11 min read

Published on: Mar 13, 2020

Last updated on: Mar 25, 2024

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Are you struggling to wrap your head around cause and effect essays? Don’t worry; you’re not alone. 

These essays might seem complex at first glance, but with the right approach, they can become easier to write.

In this comprehensive guide, we'll look into what cause and effect essays are, how to structure them, and provide valuable tips and examples to help you understand this type of writing.

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What is a Cause and Effect Essay?

A cause and effect essay is a type of essay writing that explores the relationship between events, actions, or phenomena (causes) and their outcomes or consequences (effects) . 

In this type of essay, the writer analyzes how one event leads to another, providing insights into the underlying causes and the resulting effects. Cause and effect essays aim to explain the connections between various occurrences and explain the reasons behind certain outcomes. 

They often require critical thinking, careful analysis, and the use of evidence and examples to support arguments.

You may confuse cause-and-effect essays with compare and contrast essays . While cause and effect essays focus on analyzing the relationship between events, compare and contrast essays examine similarities and differences between two or more subjects or ideas.

How to Structure a Cause and Effect Essay

There are two main structural types commonly used to write a cause and effect essay: the block structure and the chain structure.

Block Structure

In the block structure, the writer first discusses all the causes of the event in one section, followed by a separate section dedicated to discussing all the effects.

This cause and effect essay format allows for a clear separation between the causes and effects, making it easier for the reader to understand the relationships between them.

Use the block structure when:

• There are multiple causes and effects to discuss, and you want to provide a comprehensive overview of each.
• You prefer a clear separation between causes and effects for easier understanding.

Chain Structure

In the chain structure, each cause is followed immediately by its corresponding effect(s), creating a chain-like sequence of events.

This structure emphasizes the direct relationship between each cause and its effect, providing a more immediate and interconnected narrative.

Use the chain structure when:

• You want to emphasize the direct relationship between each cause and its effect.
• You're discussing a series of events that occur in a linear or chronological order.

Cause and Effect Essay Outline

Creating an outline is essential for organizing your thoughts and structuring your cause and effect essay effectively. 

Here's a basic outline to guide you through the writing process:

Need a detailed outline guide? Be sure to check out our blog on " Cause and Effect Essay Outline " for a comprehensive breakdown of how to organize your essay.

How to Write a Cause and Effect Essay

Writing a cause and effect essay involves examining the reasons (causes) and outcomes (effects) of a particular event, phenomenon, or situation. Here's a step-by-step guide to help you craft an effective cause and effect essay:

Step 1: Choose a Topic

Start by selecting a topic that interests you and has clear cause-and-effect relationships. It could be a social issue, scientific phenomenon, historical event, or any other subject with identifiable causes and effects. 

For example, "The Effects of Climate Change on Wildlife Populations" or "Causes of Obesity in Developed Countries."

Step 2: Conduct Research

Gather relevant information and evidence to support your thesis statement . Look for credible sources such as academic journals, books, government reports, and reputable websites. 

Ensure you have a thorough understanding of both the causes and effects related to your chosen topic.

Step 4: Develop a Thesis Statement

Craft a clear and concise thesis statement that outlines the main causes and effects you will discuss in your essay. Your thesis should provide a roadmap for the reader and clearly state your position on the topic. 

For instance, "The rise in carbon emissions from human activities is leading to severe consequences for global ecosystems."

Step 5: Outline your Essay

Create a structured outline that organizes your ideas and arguments logically. Divide your essay into introduction , body paragraphs (each discussing a specific cause or effect), and conclusion . 

Each body paragraph should focus on one cause or effect and provide supporting details and evidence.

Step 6: Write the Introduction

Begin with an engaging introduction that provides background information on the topic and introduces your thesis statement. 

Hook the reader's attention with an interesting fact, statistic, or anecdote related to your topic. Clearly state the purpose of your essay and preview the main points you will discuss.

Step 7: Body Paragraphs

In the body paragraphs, explore the causes or effects of the topic in detail. Start each paragraph with a topic sentence that introduces the cause or effect you will be discussing. 

Then, provide evidence and examples to support your claim. Use data, statistics, expert opinions, and real-life examples to strengthen your arguments. Make sure to explain the causal relationship between the factors you're discussing.

Step 8: Transition Between Paragraphs

Use transition words and sentences to smoothly transition between paragraphs and maintain coherence throughout your essay. 

These transitions help guide the reader through your arguments and ensure a logical flow of ideas.

Step 9: Write the Conclusion

Summarize the main points of your essay in the conclusion and restate your thesis statement. Reflect on the significance of your findings and emphasize the importance of understanding the causes and effects of the topic. 

Avoid introducing new information in the conclusion; instead, offer insights or suggestions for further research or action.

Step 10: Revise and Edit

Review your essay for clarity, coherence, and grammatical accuracy. Make sure each paragraph contributes to the overall argument and that your ideas are well-supported by evidence.

Once you've made revisions and edits, finalize your essay by formatting it according to the guidelines provided by your instructor or publication. 

Double-check citations and references to ensure they are accurate and properly formatted according to the required citation style (e.g., APA, MLA).

Cause and Effect Essay Examples

When writing a cause and effect essay for the first time, it is recommended to go through a few examples. It will help you understand the structure and how to use a method effectively.

The following are some of the great cause and effect examples free to use.

Cause and Effect Essay

Cause and Effect Essay Sample

Climate Change Cause and Effect Essay

Poverty Cause and Effect Essay

Air Pollution Cause and Effect Essay

Cause and Effect Essay Topics

Here are some cause and effect essay topics:

• The Impact of Climate Change on Extreme Weather Events
• The Rise of Mental Health Disorders Among Adolescents
• The Effects of Social Media on Political Polarization
• The Consequences of Deforestation on Biodiversity Loss
• The Relationship Between Income Inequality and Social Mobility
• The Impact of Technology on Human Relationships
• The Causes and Effects of the Global Obesity Epidemic
• The Effects of Air Pollution on Public Health
• The Impact of Artificial Intelligence on Employment
• The Causes and Consequences of Refugee Crises

These topics reflect current societal concerns and offer opportunities for in-depth analysis of cause-and-effect relationships. If you need more such ideas check out our cause and effect essay topics  blog!

Tips for Writing a Cause and Effect Essay

Here are additional tips for writing a cause and effect essay:

• Establish Clear Connections: Clearly establish the causal relationships between different factors to help readers understand the cause-and-effect dynamics of the topic.
• Avoid Oversimplification: Recognize that most events have multiple causes and effects, so avoid oversimplifying complex phenomena by considering various factors and their interactions.
• Consider Chronology: When discussing historical events, consider the chronological sequence of causes and effects to provide a clear narrative structure.
• Focus on Significance: Highlight the significance of your findings by discussing the broader implications of the causes and effects you've identified.
• Reflect and Synthesize: In the conclusion, reflect on the insights gained from analyzing the causes and effects and synthesize your findings to provide a cohesive understanding of the topic.

To conclude, writing a cause and effect essay can be a rewarding experience that allows you to look into complex issues. By following the guidelines outlined in this guide and applying your critical thinking skills, you can create compelling essays that inform and engage your audience. 

But if you are in a time crunch do not hesitate to take professional help. CollegeEssay.org provides a top cause and effect essay writing service for those students who are having a hard time meeting deadlines. We'll help you with your cause and effects essays for the best grades. 

Reach out to avail amazing discounts and get our custom essay writing help in no time. As a plus, you can use our AI writing tool if you need a quick fix to beat the deadline stress!

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How to Write a Cause and Effect Essay: Full Guide

Ever wondered how things are connected in our world? Think of the butterfly effect—where a butterfly's wings in Brazil can set off a tornado in Texas. It's a quirky idea, but it shows how events are intertwined. Writing a cause and effect essay is like unraveling these connections, connecting the dots to reveal how things influence each other and shape our experiences.

In this guide, experts from our paper writing service will explore the concept of causality and share practical tips for creating great cause and effect essays. These essays won't just provide information—they'll leave a lasting impression on your readers.

What Is a Cause and Effect Essay

A cause and effect essay is a form of writing that aims to explore and explain the relationships between different events, actions, or circumstances. The central idea is to investigate why certain things happen (causes) and what results from those occurrences (effects). It's like peeling back the layers to reveal the interconnectedness of events, understanding the domino effect in the narrative of life.

Here's a breakdown of the key components:

• Causes: These are the factors or events that initiate a particular situation. They are the reasons behind why something occurs. For instance, if you're exploring the cause of obesity, factors like unhealthy eating habits and lack of physical activity could be identified as causes.
• Effects: The effects are the outcomes or consequences that result from the identified causes. Following the obesity example, effects could include health issues, reduced quality of life, or increased healthcare costs.
• Connection: The heart of a cause and effect essay lies in demonstrating the link between causes and effects. It's not just about listing events but explaining how one event leads to another in a logical and coherent manner.

When crafting such an essay, you're essentially acting as a storyteller and investigator rolled into one. Your goal is to guide the reader through the web of interconnected events, providing insights into the 'why' and 'what happens next.'

How to Write a Cause and Effect Essay with Easy Steps

Understanding how to write a cause and effect essay is like putting together a puzzle. Here are ten simple steps to help you write an engaging essay that looks into how things are connected.

1. Select a Specific Topic

• Choose a cause and effect relationship that sparks your interest.
• Ensure your topic is focused and manageable for a thorough exploration.

2. Explore Causal Links

• Conduct thorough research to uncover hidden connections and supporting evidence.
• Look beyond the obvious to identify intricate relationships between causes and effects.

3. Craft a Clear Thesis Statement

• Develop a precise thesis that clearly articulates the main cause and the resulting effects.
• Your thesis serves as the roadmap for your essay, guiding readers through your analysis.

4. Organize Chronologically or by Significance

• Structure your essay in a logical order, either chronologically or by the significance of events.
• This organization enhances clarity and helps readers follow the cause-and-effect progression.

5. Utilize Transitional Phrases

• Employ transition words and phrases to ensure seamless flow between causes and effects.
• Clear transitions enhance readability and strengthen the coherence of your essay.

6. Support Arguments with Credible Evidence

• Back up your claims with relevant data, examples, and statistics.
• Strong evidence adds credibility to your analysis and reinforces the cause-and-effect relationships you present.

7. Illustrate Chain Reactions

• Show how a single cause can trigger a chain of effects, and vice versa.
• Illustrate the ripple effects to emphasize the complexity of the relationships.

8. Analyze Root Causes

• Move beyond surface-level explanations and explore the underlying factors contributing to the cause-and-effect scenario.
• Deep analysis adds depth and nuance to your essay.

9. Consider Alternative Causes

• Address potential counterarguments to showcase a comprehensive understanding.
• Acknowledging alternative causes strengthens your essay's overall credibility.

10. Conclude with Impact

• Summarize key points and emphasize the broader significance of your analysis.
• Leave your readers with a thought-provoking conclusion that ties together the cause-and-effect relationships explored in your essay.

Cause and Effect Essay Structure Types

When setting up your essay, you can choose from different structures to make it organized. Let's look at two common types of cause and effect essay structures:

• Block Structure:

The block structure is a clear and organized way to present causes and effects in your essay. Here, you dedicate one section to discussing all the causes, covering multiple causes within each category. After that, you have another section to explore all the effects. This separation makes your ideas easy to understand.

Using the block structure allows you to dive deep into each category, thoroughly looking at causes and effects separately. It's handy when you want to give a detailed analysis and show the importance of each part of the causal relationship. This way, readers can fully grasp each element before moving on.

• Chain Structure:

On the other hand, the chain structure focuses on how events are connected and create ripple effects. It highlights how one cause leads to a specific effect, and that effect becomes the cause of more effects in an ongoing chain. This method is potent for illustrating the complexity of causal relationships.

The chain structure works well when you want to emphasize the sequence of events or deal with intricate cause-and-effect scenarios. It allows you to show how actions trigger a series of reactions, displaying the domino effect that leads to a specific outcome.

Regardless of the structural style you choose, if you require assistance with your academic paper, reach out to us with your ' write my paper for me ' request. Our experienced team is ready to tailor your paper to your specific requirements and ensure its excellence.

Cause and Effect Essay Outline

Creating an effective cause and effect essay begins with a well-structured outline. This roadmap helps you organize your thoughts, maintain a logical flow, and ensure that your essay effectively conveys the causal relationships between events. Below, we'll outline the key components of the essay along with examples:

I. Introduction

• Hook: Start with an engaging statement or fact. Example: 'Did you know that stress can significantly impact your overall health?'
• Background Information: Provide context for your topic. Example: 'In today's fast-paced world, stress has become an increasingly prevalent issue.'
• Thesis Statement: Clearly state the main cause and its corresponding effects. Example: 'This essay will explore the causes of stress and their profound negative effects on physical and mental health.'

II. Body Paragraphs

• Topic Sentence: Introduce the first cause you'll discuss. Example: 'One major cause of stress is heavy workload.'
• Supporting Details: Provide evidence and examples to support the cause. Example: 'For instance, individuals juggling multiple job responsibilities and tight deadlines often experience heightened stress levels.'
• Transition: Link to the next cause or move on to the effects.
• Topic Sentence: Introduce the first effect. Example: 'The effects of chronic stress on physical health can be devastating.'
• Supporting Details: Present data or examples illustrating the impact. Example: 'Studies have shown that prolonged stress can lead to cardiovascular problems, including hypertension and heart disease.'
• Transition: Connect to the next effect or cause.

C. Causes (Continued)

• Topic Sentence: Introduce the next cause in a new cause and effect paragraph. Example: 'Another significant cause of stress is financial strain.'
• Supporting Details: Explain how this cause manifests and its implications. Example: 'Financial instability often results in anxiety, as individuals worry about bills, debts, and their financial future.'
• Transition: Prepare to discuss the corresponding effects.

D. Effects (Continued)

• Topic Sentence: Discuss the effects related to financial strain. Example: 'The psychological effects of financial stress can be profound.'
• Supporting Details: Offer real-life examples or psychological insights. Example: 'Depression and anxiety are common consequences of constant financial worries, affecting both mental well-being and daily life.'

III. Conclusion

• Restate Thesis: Summarize the main cause and effects. Example: 'In summary, the heavy workload and financial strain can lead to stress, impacting both physical and mental health.'
• Closing Thoughts: Reflect on the broader significance of your analysis. Example: 'Understanding these causal relationships emphasizes the importance of stress management and financial planning in maintaining a balanced and healthy life.'

Cause and Effect Essay Examples

To help you grasp cause and effect essay writing with clarity, we have prepared two distinct essay examples that will guide you through the intricacies of both block and chain structures. Additionally, should you ever find yourself requiring assistance with academic writing or descriptive essays examples , simply send us your ' write my research paper ' request. Our expert writers are here to provide the support you need!

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Cause and Effect Essay Topics

Choosing a good topic starts with recognizing cause and effect key words. Here are 10 interesting topics that let you dig into fascinating connections and their important consequences:

• The Relationship Between Lack of Exercise and Mental Health in Older Adults
• Effects of Sleep Deprivation on Workplace Productivity
• The Impact of Cyberbullying on Adolescents' Emotional Well-being
• Influence of Social Media Advertising on Consumer Purchasing Decisions
• Consequences of Oil Spills on Coastal Ecosystems
• How Noise Pollution Affects Concentration and Academic Performance in Schools
• The Connection Between Fast-Food Marketing and Childhood Obesity
• Effects of Urbanization on Water Quality in Local Rivers
• The Relationship Between Indoor Plants and Air Quality in Homes
• Impact of Plastic Pollution on Wildlife in Urban Environments
• The Effect of Meditation on Stress Reduction in College Students
• How Increased Screen Time Affects Teenagers' Attention Span
• The Impact of Single-Use Plastics on Marine Microorganisms
• The Relationship Between Smartphone Use and Sleep Quality in Adults
• Effects of High-Fructose Corn Syrup on Metabolic Health
• The Consequences of Deforestation on Local Biodiversity
• Influence of Social Media Comparison on Body Dissatisfaction in Adolescents
• The Connection Between Air Pollution and Respiratory Health in Urban Areas
• Effects of Excessive Gaming on Academic Performance in High School Students
• The Impact of Fast Food Consumption on Childhood Obesity Rates

Final Words

Knowing what a cause and effect essay is and how to write it helps you uncover connections in different topics. With this guide, you can share your ideas in a clear and impactful way.

Meanwhile, if you're in need of a reaction paper example , rest assured we have you covered as well. So, seize this opportunity, put your thoughts on paper logically, and witness your essays leaving a lasting and influential mark.

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is a seasoned educational writer focusing on scholarship guidance, research papers, and various forms of academic essays including reflective and narrative essays. His expertise also extends to detailed case studies. A scholar with a background in English Literature and Education, Daniel’s work on EssayPro blog aims to support students in achieving academic excellence and securing scholarships. His hobbies include reading classic literature and participating in academic forums.

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Cause and Effect Essay Outline: Types, Examples and Writing Tips

20 June, 2020

9 minutes read

Author:  Tomas White

This is a complete guide on writing cause and effect essays. Find a link to our essay sample at the end. Let's get started!

What is a Cause and Effect Essay?

A cause and effect essay is the type of paper that the author is using to analyze the causes and effects of a particular action or event. A curriculum usually includes this type of exercise to test your ability to understand the logic of certain events or actions.

If you can see the logic behind cause and effect in the world around you, you will encounter fewer problems when writing. If not, writing this kind of paper will give you the chance to improve your skillset and your brain’s ability to reason.

“Shallow men believe in luck or in circumstance. Strong men believe in cause and effect.” ― Ralph Waldo Emerson

In this article, the  Handmade Writing team will find out how to create an outline for your cause and effect essay – the key to successful essay writing.

Types of the Cause and Effect Essay

Before writing this kind of essay, you need to draft the structure. A good structure will result in a good paper, so it’s important to have a plan before you start. But remember , there’s no need to reinvent the wheel: just about every type of structure has already been formulated by someone.

If you are still unsure about the definition of an essay, you can take a look at our guide:  What is an Essay?

Generally speaking, there are three types of cause and effect essays. We usually differentiate them by the number of and relationships between the different causes and the effects. Let’s take a quick look at these three different cases:

1. Many causes, one effect

This kind of essay illustrates how different causes can lead to one effect. The idea here is to try and examine a variety of causes, preferably ones that come from different fields, and prove how they contributed to a particular effect. If you are writing about World War I, for example, mention the political, cultural, and historical factors that led to the great war.

By examining a range of fundamental causes, you will be able to demonstrate your knowledge about the topic.

Here is how to structure this type of essay:

• Introduction
• Cause #3 (and so on…)
• The effect of the causes

2. One cause, many effects

This type of cause and effect essay is constructed to show the various effects of a particular event, problem, or decision. Once again, you will have to demonstrate your comprehensive knowledge and analytical mastery of the field. There is no need to persuade the reader or present your argument . When writing this kind of essay, in-depth knowledge of the problem or event’s roots will be of great benefit. If you know why it happened, it will be much easier to write about its effects.

Here is the structure for this kind of essay:

• Effect #3 (and so on…)

3. Chain of causes and effects

This is the most challenging type. You need to maintain a chain of logic that demonstrates a sequence of actions and consequences, leading to the end of the chain. Although this is usually the most interesting kind of cause and effect essay, it can also be the most difficult to write.

Here is the outline structure:

• Effect #1 = Cause #2
• Effect #2 = Cause #3
• Effect #3 = Cause #4 (and so on…)

Cause and Effect Essay Outline Example

Let’s take a look at an example. Below, you will find an outline for the topic “The causes of obesity” (Type 1) :

As you can see, we used a blended strategy here. When writing about the ever-increasing consumption of unhealthy food, it is logical to talk about the marketing strategies that encourage people to buy fast food. If you are discussing fitness trainers, it is important to mention that people need to be checked by a doctor more often, etc.

In case you face some issues with writing your Cause and Effect essay, you can always count on our Essay Writers !

How do I start writing once I have drafted the structure?

If you start by structuring each paragraph and collecting suitable examples, the writing process will be much simpler. The final essay might not come up as a classic five paragraph essay – it all depends on the cause-effect chain and the number of statements of your essay.

In the Introduction, try to give the reader a general idea of what the cause and effect essay will contain. For an experienced reader, a thesis statement will be an indication that you know what you are writing about. It is also important to emphasize how and why this problem is relevant to modern life. If you ever need to write about the Caribbean crisis, for instance, state that the effects of the Cold War are still apparent in contemporary global politics. 

Related Post: How to write an Essay introduction | How to write a Thesis statement

In the Body, provide plenty of details about what causes led to the effects. Once again, if you have already assembled all the causes and effects with their relevant examples when writing your plan, you shouldn’t have any problems. But, there are some things to which you must pay particular attention. To begin with, try to make each paragraph the same length: it looks better visually. Then, try to avoid weak or unconvincing causes. This is a common mistake, and the reader will quickly realize that you are just trying to write enough characters to reach the required word count.

Moreover, you need to make sure that your causes are actually linked to their effects. This is particularly important when you write a “chained” cause and effect essay (type 3) . You need to be able to demonstrate that each cause was actually relevant to the final result. As I mentioned before, writing the Body without preparing a thorough and logical outline is often an omission.

The Conclusion must be a summary of the thesis statement that you proposed in the Introduction. An effective Conclusion means that you have a well-developed understanding of the subject. Notably, writing the Conclusion can be one of the most challenging parts of this kind of project. You typically write the Conclusion once you have finished the Body, but in practice, you will sometimes find that a well-written conclusion will reveal a few mistakes of logic in the body!

Cause and Effect Essay Sample

Be sure to check the sample essay, completed by our writers. Use it as an example to write your own cause and effect essay. Link: Cause and effect essay sample: Advertising ethic issues .

Tips and Common Mistakes from Our Expert Writers

Check out Handmadewriting paper writing Guide to learn more about academic writing!

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How to Write a Cause and Effect Essay

Published September 27, 2020. Updated May 19, 2022.

Cause and Effect Essay Definition

A cause and effect essay explains why events happen (causes), what results (effects), and the relationship between the cause and effect(s).

Overview of a Cause and Effect Essay

Cause and effect essays are commonly structured in four ways: causal chain, causes, effects, and causes and effects. Once you decide on a structure, you should choose your topic. You may already have some causes and/or effects in mind. Brainstorm to come up with ideas. Brainstorming helps you think more about your topic and gives you a good selection of causes and effects to choose from. Choose what causes and effects to focus on. Develop a discussion of the causes and effects to build a case for the plausibility of these causes and effects and their relationship.

Worried about your writing? Submit your paper for a Chegg Writing essay check , or for an Expert Check proofreading . Both can help you find and fix potential writing issues.

Step 1: Choose a Focus

Cause and effect essays are commonly structured in four ways:

• Causal chain
• Causes & effects

Start by considering the length of your essay and other requirements. Follow the focus and topic assigned by your instructor. Otherwise, choose the option that is best for you.

Causal Chain

A causal chain follows a specific sequence of causes and effects. It starts with an initial topic and then moves forward, identifying a specific effect of this topic. This effect, then, causes another effect, and so on down the chain.

Topic → leads to A → leads to B → leads to C → final effect

A causal chain is a good structure if you want to build up to a certain key effect of the topic and show the reader the steps it takes to get there.

The causal chain structure works well for either a short (2-3 pages) or a long (4+ pages) essay, depending on how many steps you need to discuss to reach the final effect.

When you focus on causes, start with a topic you’re interested in and think about what caused it? In a way, you’re looking backward to understand the factors that caused something or that keep it happening.

Causes → Topic

This is good for a short essay because the scope is limited to focusing on causes.

If you focus on effects, start with a topic and work forward by asking what happens due to this event or topic? What are its effects?

Topic → Effects

Effects may be in the future. For example, if a certain law is passed, what will be the most likely outcome? We can’t know for sure until it happens, but we can use existing factors and logical reasoning to make a case for certain possibilities.

You could also focus on effects that are occurring or that have occurred. For example, what effects do video games have on a certain age group? This might also allow you to focus your analysis on an existing debate. In this example, the nature of the effects of video games on children is a common topic of debate.

This is good for a short essay because what you are covering is limited to effects.

Causes and Effects

With this focus, you’d consider what makes something happen and what its effects are.

Causes → Topic → Effects

If you are writing a longer essay, you could consider discussing both causes and effects. This wider scope could result in a more thorough examination of the topic. But make sure not to set yourself up to do too much. You don’t have to touch on every cause and effect you brainstorm. Rather, your focus should relate to your purpose. Remembering your focus allows you to screen out the causes and effects that aren’t relevant to your purpose.

The cause and effect structure is good for a longer essay (4 or more pages) because you’ll have to cover more material.

Step 2: Choose a Topic

Now that you’ve decided on a focus, what do you want to write about? Your assignment prompt might give you some direction, but if the essay is open-topic, consider what you’d be interested in writing about. Here are some ideas to help you choose:

Consider Your Purpose

You want to have an end goal, a purpose. You’re discussing causes and effects, but why? To show people what? To convince people of what? For example, you could analyze effects for the purpose of showing that video games help teenagers develop good teamwork and decision-making skills.

At first, you might think about what you want to learn or explore. Maybe you’ve found that jobs in a career field you’re interested in are increasing or decreasing, and you’d like to explore the causes for that. Maybe you’d like to explore the effects of companies allowing employees to work from home. If your research leads you to conclude that these effects are mostly positive, you might focus your purpose on convincing employers to offer more work-from-home flexibility. To do that, you’d analyze the effects.

Consider Your Audience

Consider your audience can help you focus your topic and develop content. What are the relevant characteristics of your audience? What are their likely questions, concerns, or biases? Answering these questions helps you decide what to focus on. If your audience is owners or leaders of a struggling business, you could analyze the causes of their poor sales to help them improve. This example shows the connection between audience and purpose.

A phenomenon is something noteworthy or special that stands out. The topic could be from pop culture, science, current events, or anything else. You could make an argument for the causes of a movie’s popularity or explore why a particular age group favors a certain social media platform. Topics are everywhere!

Trend , as used here, doesn’t mean a fad, but rather, something that rises or falls in popularity over time.

If you write on a trend, decide the beginning and end of the period you will be discussing. For instance, the rise of women in the workforce starting from WWII makes sense because with men fighting in the war, women had to step into several key industries normally dominated by men. However, if you tried to discuss significant causes of the increase of women in the workforce from WWII to the present, you’d probably find that to be too long of a period of time to discuss thoroughly.

Step 3: Brainstorm Causes and Effects

You may already have some causes and effects in mind. Keep brainstorming to come up with more. You won’t write about everything, but brainstorming helps you think more about your topic and gives you a good selection of causes and effects to choose from.

As you brainstorm, consider different types of causes and effects.

Surface Causes and Effects

Surface causes and effects are obvious. They come immediately to mind, and their connection to the topic is clear or well-known. For example, the connection between smoking and lung damage.  Because of this, surface causes and effects usually don’t need extensive development. While they could have a role in your essay, you wouldn’t want to focus solely on obvious causes and effects.

Below-the-Surface Causes and Effects

These are not immediately obvious. This doesn’t mean they’re baseless “conspiracy theory” ideas, but that they’re not things people would immediately know or think of. They might be more complicated or even rarely acknowledged on a conscious level. These might not even occur to you until you’ve done more research and thought more about the topic. Below-the-surface causes and effects take more work to develop in an essay, but they are generally more intriguing.

Immediate Causes and Effects

Immediate causes and effects happen right before or after the topic. Because of this proximity, they are often more obvious, although they are not necessarily simple.

Remote or Background Causes and Effects

These happen well before or after the topic. You’ll have to think about the length of time that makes sense for your topic. If you are considering the increase of women in the workforce, considering WWII probably makes sense, even though it was over seventy years ago. However, if you are speculating about the causes of the popularity of Facebook, seventy years in the past is too far.

Perpetuating Causes

Perpetuating causes not only make something happen but also keep it going as well. Such causes perpetuate the topic.

Step 4: Choose What Causes and Effects to Focus On

Use these ideas to help you decide what causes and effects to focus on:

• Does your prompt tell you how many causes and effects to cover? Make sure to follow assignment instructions.
• Choose causes and effects that help you accomplish your purpose.
• Choose causes and effects relevant to your audience.
• You might notice that certain causes/effects cluster around a particular idea or theme. You could choose to focus on that theme.
• What types of causes and effects did you brainstorm? It will take more effort and writing space to develop an argument for the plausibility of a below-the-surface cause than a surface cause. Don’t take on more complicated causes and effects than you can develop in your page range.
• Don’t go the route of using lots of obvious causes and effects. These won’t give you the chance to develop an in-depth analysis and your paper might end up more like a list.

Before you turn in that paper, don’t forget to cite your sources in APA format , MLA format , or a style of your choice.

Step 5: Develop a Discussion of Your Causes and Effects

You are looking for connections between the causes and the effects of the topic. You’re building a case for the plausibility of these causes and effects.

Have a working thesis in mind. You’ll probably refine it as you go.

Make sure to avoid the false causality logical fallacy . This can also be expressed as “coincidence doesn’t equal causation.” That one event precedes another does not make the first event a cause of another. It’s up to you as the writer to establish a firm causal link.

Think about the order in which you present the causes and effects. There might be some that form a foundation for understanding others. There might also be a chronological sequence, especially if you are following a causal chain. You might also choose to develop your most compelling cause or effect.

Example Cause and Effect Essay on the Internet’s Influence on Young Adults

By Ericka Scott Nelson. Ericka earned a MA in English from the University of California, Riverside. She teaches composition at a community college.

Common Writing Assignments, Apps & Tests

• Analytical Essay
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• Book Report
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• Cause and Effect Essay
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Cause and Effect in Composition

Glossary of Grammatical and Rhetorical Terms

• An Introduction to Punctuation
• Ph.D., Rhetoric and English, University of Georgia
• M.A., Modern English and American Literature, University of Leicester
• B.A., English, State University of New York

In composition , cause and effect is a method of paragraph or essay development in which a writer analyzes the reasons for—and/or the consequences of—an action, event, or decision.

A cause-and-effect paragraph or essay can be organized in various ways. For instance, causes and/or effects can be arranged in either chronological order or reverse chronological order. Alternatively, points can be presented in terms of emphasis , from least important to most important, or vice versa.

Examples and Observations

• "If you prove the cause , you at once prove the effect ; and conversely nothing can exist without its cause." (Aristotle, Rhetoric )
• Immediate Causes and Ultimate Causes "Determining causes and effects is usually thought-provoking and quite complex. One reason for this is that there are two types of causes: immediate causes , which are readily apparent because they are closest to the effect, and ultimate causes , which, being somewhat removed, are not so apparent and may perhaps even be hidden. Furthermore, ultimate causes may bring about effects which themselves become immediate causes, thus creating a causal chain . For example, consider the following causal chain: Sally, a computer salesperson, prepared extensively for a meeting with a client (ultimate cause), impressed the client (immediate cause), and made a very large sale (effect). The chain did not stop there: the large sale caused her to be promoted by her employer (effect)." (Alfred Rosa and Paul Eschholz, Models for Writers , 6th ed. St. Martin's Press, 1998)
• Composing a Cause/Effect Essay "For all its conceptual complexity, a cause/effect essay can be organized quite simply. The introduction generally presents the subject(s) and states the purpose of the analysis in a clear thesis . The body of the paper then explores all relevant causes and/or effects, typically progressing from least to most influential or from most to least influential. Finally, the concluding section summarizes the various cause/effect relationships established in the body of the paper and clearly states the conclusions that can be drawn from those relationships." (Kim Flachmann, Michael Flachmann, Kathryn Benander, and Cheryl Smith, The Brief Prose Reader . Prentice Hall, 2003)
• Causes of Child Obesity "Many of today's kids are engaged in sedentary pursuits made possible by a level of technology unthinkable as recently as 25 to 30 years ago. Computer, video, and other virtual games, the ready availability of feature films and games on DVD, plus high-tech advancements in music-listening technology have come down into the range of affordability for parents and even for the kids themselves. These passive pursuits have produced a downside of reduced physical activity for the kids, often with the explicit or implicit consent of the parents. . . . "Other fairly recent developments have also contributed to the alarming rise in child obesity rates. Fast food outlets offering consumables that are both low in price and low in nutritional content have exploded all over the American landscape since the 1960s, especially in suburban areas close to major highway interchanges. Kids on their lunch breaks or after school often congregate in these fast food outlets, consuming food and soft drinks that are high in sugar, carbohydrates, and fat. Many parents, themselves, frequently take their children to these fast food places, thus setting an example the kids can find justification to emulate." (MacKie Shilstone, Mackie Shilstone's Body Plan for Kids . Basic Health Publications, 2009)
• Cause and Effect in Jonathan Swift's "A Modest Proposal" "'A Modest Proposal' is a brilliant example of the use of non-argumentative devices of rhetorical persuasion . The whole essay, of course, rests broadly upon the argument of cause and effect : these causes have produced this situation in Ireland, and this proposal will result in these effects in Ireland. But Swift, within the general framework of this argument, does not employ specific argumentative forms in this essay. The projector chooses rather to assert his reasons and then to amass them by way of proof ." (Charles A. Beaumont, Swift's Classical Rhetoric . Univ. of Georgia Press, 1961)
• Effects of Automobiles "I worry about the private automobile. It is a dirty, noisy, wasteful, and lonely means of travel. It pollutes the air, ruins the safety and sociability of the street, and exercises upon the individual a discipline which takes away far more freedom than it gives him. It causes an enormous amount of land to be unnecessarily abstracted from nature and from plant life and to become devoid of any natural function. It explodes cities, grievously impairs the whole institution of neighborliness, fragmentizes and destroys communities. It has already spelled the end of our cities as real cultural and social communities, and has made impossible the construction of any others in their place. Together with the airplane, it has crowded out other, more civilized and more convenient means of transport, leaving older people, infirm people, poor people and children in a worse situation than they were a hundred years ago." (George F. Kennan, Democracy and the Student Left , 1968)
• Examples and Effects of Entropy "Because of its unnerving irreversibility, entropy has been called the arrow of time. We all understand this instinctively. Children's rooms, left on their own, tend to get messy, not neat. Wood rots, metal rusts, people wrinkle and flowers wither. Even mountains wear down; even the nuclei of atoms decay. In the city we see entropy in the rundown subways and worn-out sidewalks and torn-down buildings, in the increasing disorder of our lives. We know, without asking, what is old. If we were suddenly to see the paint jump back on an old building, we would know that something was wrong. If we saw an egg unscramble itself and jump back into its shell, we would laugh in the same way we laugh as a movie run backward." (K.C. Cole, "The Arrow of Time." The New York Times , March 18, 1982)
• Affect vs. Effect: How to Choose the Right Word
• Understanding General-to-Specific Order in Composition
• Definition and Examples of the Topoi in Rhetoric
• What Is an Annotation in Reading, Research, and Linguistics?
• How to Use Exemplification in Writing
• Polemic: Definition and Examples
• Learn How to Use Extended Definitions in Essays and Speeches
• Understanding Organization in Composition and Speech
• Periodical Essay Definition and Examples
• What Does It Mean to Make a Claim During an Argument?
• Definition and Examples of Formal Essays
• Definition and Examples of Propaganda
• Definition and Examples of Humorous Essays
• Organizational Strategies for Using Chronological Order in Writing
• Definition Examples of Collage Essays

How to Write a Cause and Effect Essay

Writing essays is inevitable for all students. And while many of them consider this kind of academic assignment difficult and boring, others truly enjoy writing their essays on the widest array of topics. Do you want to know their secret? It’s simple: they just know how to write essays well! And those who don't also have a solution – they are ready to pay for essay best services to get completed paper without a hassle. Finding the essay writing service out there to fall back on is great but honing your own writing skills will never go amiss.

If you are reading this article, then you’re already on your way to start loving essay writing. By the time you finish reading it, you will have all the necessary instruments at hand to craft an impressive essay of one particular type – that is, a cause and effect essay (sometimes also called cause-effect or reason and result essay).

What Is a Cause and Effect Essay?

It is impossible to do something well without knowing what exactly it is that you have to do. So, let’s start with the basics – the cause and effect essay definition.

A cause and effect essay (also called cause-effect or reason and result essay) is a type of an analytical academic paper in which the relationship between causes and effects of a particular event or phenomenon is being analyzed. It usually answers the questions, “why?” (cause) and “what is the result?” (effect), and utilizes subjunctive mood extensively. If already at this moment you feel you're unlikely to be able to cope with writing an essay yourself – relax and get help from professional dissertation writing services .

How to Make a Correct Cause and Effect Essay Structure

Now that we know what a cause and effect essay is, we can start working on its structure. Having a clear structure is essential for the successful completion of your assignment. So, it’s highly important to devote enough time to this part of the task. If you think it's pretty challenging for you or you simply don't want to spend time on it, you can always look for coursework writing help , custom essay writing and get help from experts in the field.

There are two main ways to structure a cause and effect essay – using a block or a chain pattern. Your essay outline will differ depending on what option you choose.

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Cause and Effect Essay Outline

A cause and effect essay outline consists of a minimum of four sections – an introduction, at least two body paragraphs, and a conclusion. Each section, in turn, consists of several parts, and their contents vary depending on what pattern – block or chain – you choose.

Let’s start with a block structure.  This is how it will look like:

• Introduction;
• Body paragraph I: cause;
• Body paragraph II: effect;
• Conclusion.

Depending on your topic and approach, you can focus more on the effects or the causes and have various numbers of both. For example, if you put the main focus on the effects, your outline may look like this:

• Body paragraph I: effect #1;
• Body paragraph II: effect #2;
• Body paragraph III: cause;

If you choose the chain pattern, it will mean that in your body paragraphs, every cause will be immediately followed by its effect. The outline will then be as follows:

• Body paragraph I: cause #1 -> effect #1;
• Body paragraph II: cause #2 -> effect #2;   

In this case, too, the numbers of causes and effects may vary – it is their sequence that matters.

Now, let’s look closer at every section of the structure.

Introduction

Every essay starts with an introduction. In this section, you must introduce your topic to the reader, give some background information, and explain how you’re going to approach the discussion.

This is what an introduction section of a cause and effect essay must include:

• Background information;
• Thesis statement.

If you’re wondering how to start a cause and effect essay, you can use some of the proven techniques like using a quote, a rhetorical question, or a statement that is surprising or paradoxical. Then, after giving some background information, move on to a thesis statement.

A thesis is the part of your essay in which the main point of discussion is stated. It should be clear and concise and allow no ambiguity.

Example: “The gender gap is still very far from being closed. Globally, gender parity stands at 68.6%, according to the Global Gender Gap Report (2020). In this essay, we’ll look closely at some of the causes and effects of this phenomenon”.

Body Paragraphs (Causes)

Depending on what type of structure you choose, your body paragraphs may be slightly different. But, in any case, they should contain the following elements:

• thesis (main cause or effect);
• arguments (evidence);
• conclusion, and transition to the next section.

These may be arranged in a different way, but their presence is essential. Let’s again turn to our gender inequality topic and see how it works. In the causes section, we will list the various causes of the discussed phenomena:

• Cause #1 – societal mindset;
• Cause #2 – lack of sufficient childcare;
• Cause #3 – lack of political representation.

Each of these causes should be supported by evidence to be persuasive to the reader. This is how it may be put in a paragraph:

“One of the main causes of such inequality is the societal mindset that still regards women as primarily being responsible for providing home comfort and childcare. Most men still expect their wives to stay at home and sacrifice their careers in order to take the majority of household responsibilities (support with evidence – statistical figures, etc.).

Treat the next causes in the same manner.

Body Paragraphs (Effects)

This paragraph is basically the same as the previous one, with the only difference that here, we will discuss the effects of the phenomenon. Let’s continue with our topic:

• Effect #1 – higher levels of frustration;
• Effect #2 – lower income;
• Effect #3 – feelings of insecurity and vulnerability.

Keep in mind that the effects must be direct consequences of your causes – you can’t just pick random facts. You should also make that connection clear in your text.

Example: “Such prejudiced societal mindset regarding women and their role in the society results in higher levels of frustration among women. They feel that they have reached their glass ceiling just because of the fact that they have been born female – i.e., something they just couldn’t affect in any way (support with evidence)”.

Then, go on in the same manner in the next body-effects paragraphs.

After you’ve discussed all the causes and effects that you planned, continue with making a short conclusion. It must contain the following points:

• Reiteration of your thesis;
• Short summary of the essay’s key points;
• Concluding afterthoughts.

This is what it will look like in our case:

“As we see, gender inequality is still a pressing issue in the modern world, and it’s far from being solved. This phenomenon has multiple causes, the most obvious of which are society’s prejudiced attitude, lack of childcare, and lack of political representation for women. The effects of these problems are plausible: women end up feeling frustrated, having lower income, and being generally vulnerable. In order to change the situation, we mustn’t avoid discussions of this issue and should try to find solutions to the problems that cause it”.

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Interesting Cause and Effect Essay Topics

If you’re looking for an interesting topic for cause and effect essay, this section is for you. Listed below are some good cause and effect essay topics on various popular themes – history, politics, society, and more. Use them as examples to brainstorm ideas of your own.

History and politics:

• The economic consequences of the Civil War in the U.S.
• The collapse of the Soviet Union and its effect on the world’s power balance.
• World War II and its effect on the world economy.
• Brexit: was it necessary and how it will affect the U.K.
• Gender inequality as a major source of stress for modern women.
• How having children changes the life of a family.
• Social media as the major source of procrastination for students.
• Why do people commit crimes?
• How outstanding writing skills can help your future career.
• Burnout at work as a major career threat.
• Why it is important to go to college.
• Starting a business as a student. How it can affect your studies and future career.  

Environment:

• Air pollution as one of the main threats to public health.
• The effects of COVID-19 pandemic on the environment.
• How melting glaciers in the Arctic affect climate change on our planet.
• Multiple effects of global warming on the Earth’s population.
• Why we all need to go green right now.

Cause and Effect Essay Examples

Now that you have all the tools necessary to create a good cause and effect essay of your own let’s look at an example to see how all the components work together. Let’s assume that our topic is “Procrastination among college students.” Here, we will use a block structure, and this is how our example cause and effect essay will look like.

Procrastination Among College Students.

Our first paragraph is an introduction. Here we introduce our topic with a hook statement, give some background information, and make a thesis statement. 

Procrastination is dangerous for college students. At the same time, it’s extremely common among them: various studies show that up to 95% of college students engage in it from time to time, and almost 50% do this systematically. The causes of this phenomenon are multi-faceted and profound, and it’s vital to discover them in every particular case to be able to fight procrastination effectively. But to start treating procrastination as a problem, students must be aware of its harmful consequences. There are many of them, but one of the most acute ones for college students is its negative effect on their academic performance.

Here, the topic suggests that we have to focus more on the effects than on the causes, so the first body paragraph will be about an effect mentioned in the title. First, we will name the effect and then bring arguments and evidence to support our claim.

Procrastination is putting off things one has to do till the last minute and spending one’s time on some other, less important occupations. When students procrastinate instead of doing their academic assignments, they usually end up not having enough time to complete their tasks properly by the deadline. As a result, they only do what they can in the amount of time left, and the quality of their work may suffer. For most students, it means receiving lower grades than they could have achieved had they spent their time more wisely. And this is not a mere assumption: a study conducted by Warwick Business School has proven that procrastination leads students to lower grades (2019). One may argue that it depends largely on how gifted a student is, but even the talented ones may get to the point when the assignment is so difficult that they cannot do it well quickly.

Our second body paragraph will be about another effect. We will write it using the same scheme as in the previous paragraph.

What’s worse, procrastination can also cause mental health problems among students (Source, year). When a person finds out that they only have several hours to complete an assignment that requires several days to be done well, they are most likely to succumb to anxiety. Science proves this, too: for example, a 2010 study titled “I’ll Go to Therapy, Eventually” found a clear connection between procrastination and poorer mental health. Then, worries about failing to do a task properly resulted in even more anxiety and stress, and if a student eventually gets a lower grade than expected, it may lead to a feeling of guilt, regret, and even to depression, especially if the situation is repeated often.

In the third body paragraph, we will talk about the causes. 

It may be tempting to just label students who keep putting off their assignments as sluggards, but there are more complex and profound reasons for procrastination than mere laziness. As A. Chris Heath, MD, a psychiatrist from Dallas, says, procrastination usually happens because the task seems too difficult. It can also be an issue of self-esteem, he adds, – when a person thinks he or she is not good enough to cope with a demanding task. There are many other causes for procrastination among students, like having trouble concentrating or not possessing enough organizational skills. But whatever the reasons are, the results procrastination leads to are always devastating.

Conclusion. Here, we reiterate our thesis, site the significance of the topic, and add some afterthoughts.

As we see now, procrastination is a huge problem for college students. Being considered a result of pure laziness by many, it is often overlooked as a common problem. But this approach can be very dangerous.

In reality, procrastination has deeper roots, and the effects it causes are quite harmful. If treated lightly, systematic procrastination eventually leads college students to lower grades, mental health problems, and poorer overall academic performance.

So, it’s essential for every college student not to ignore the problem and find the causes of procrastination in their particular case as early as possible to be able to avoid its dreadful consequences.

That’s it! Feel free to use this essay as a model to generate your unique cause and effect essay ideas. If you need another example, download cause and effect essay sample here.   

Wrapping Up

In this article, we’ve covered all the important issues on how to write a cause and effect essay. After reading it thoroughly, you should know what a cause and effect essay is, how to structure it well, and make an outline that will work. We’ve also explained how to work on every paragraph of your text and provided some good essay topics as well as examples of a cause and effect essay with commentary. 

Still puzzled about how to write your cause and effect essay properly? Get instant write a paper for me help from professional editors and writers.  With such detailed instruction, you cannot fail, if you are diligent enough to practice writing essays on your own using the information given. Don’t get downhearted if you won’t be able to write a flawless paper from the first try; remember: practice makes perfect. So, put effort into your essay writing, and this will pay you back in the future – not only with excellent marks but with better critical thinking and logical skills, too.

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• Academic practice
• General practice
• Task 1 Academic
• Task 1 General
• Task 2 (essay)

How to write cause/effect essays in IELTS?

Cause and effect essay questions in IELTS Writing task 2 give you a problem and ask you to state the main causes of this problem and discuss its possible effects .

In this lesson you will see:

• how to generate ideas for causes and effects
• band 9 answer structure for causes/effects essay
• cause/effect model essay

This is an example of cause/effect IELTS writing task 2 question:

Today more people are overweight than ever before.

What in your opinion are the primary causes of this?

What are the main effects of this epidemic?

Generating ideas

After you’ve read the question, you can clearly determine the problem: growing number of overweight people .

But before you start to write your essay, it’s a good idea to think of 2-3 causes and 2-3 possible effects of the problem.

Causes of obesity :

• inactive lifestyle (relying on cars instead of walking, fewer physical demands at work, inactive leisure activities)
• unhealthy eating habits (eating fast-food, drinking high-calorie beverages, consuming large portions of food, eating irregularly)

Effects of obesity :

• physical health problems
• loss of productivity
• depressions and mental disorders

Now, after we’ve generated the main ideas for causes and effects, it’s time to use these ideas in our essay.

Band 9 answer structure

As you know, there are many ways to structure your essay, but we’ll use a structure that has been approved by many IELTS examiners to be high-scoring and coherent .

Band-9 essay structure :

Introduction

Body paragraph 1 - causes

Body paragraph 2 - effects

Let’s take a look at each of these sections in detail.

Write your introduction in two sentences:

Nowadays the number of overweight people is constantly growing.

This essay will discuss the main reasons of this epidemic and then describe the possible effects of the problem.

In my opinion, the foremost causes of obesity are inactive lifestyle and unhealthy eating habits.

Today more and more people rely on cars instead of walking, have less physical demands at work and prefer inactive leisure activities. This results in burning less calories and gaining weight.

Moreover, the problem is accentuated by the growing number of people, who eat irregularly and consume large portions of high-calorie food. For example, about 50% of the adult population in Europe with so-called disordered eating suffer from obesity.

The possible effects of this problem include physical health problems and loss of productivity.

First of all, obesity results in incorrect functioning of the human body and contributes to the risk of developing some chronic illnesses. For example, as body fat percentage increases, the person’s metabolism worsens, which in turn may result in diabetes or heart diseases.

Secondly, overweight people are very unhealthy and often suffer from stress and tiredness. This lessens their work capacity and results in lower productivity. For example, it has been proven that an obese person needs to put more effort to complete some task than a person with normal weight.

For the conclusion you need simply to restate the problem and sum up the causes and effects that you described in your body paragraphs:

To sum up, obesity is a big problem that affects a lot of people nowadays. It’s mainly caused by inactive lifestyle and eating disorders and results in severe health problems and loss of productivity.

Model essay

Nowadays the number of overweight people is constantly increasing. This essay will discuss the main reasons of this epidemic and then describe the possible effects of the problem.

In my opinion, the foremost causes of obesity are inactive lifestyle and unhealthy eating habits. Today more and more people rely on cars instead of walking, have less physical demands at work and prefer inactive leisure activities. This results in burning less calories and gaining weight. Moreover, the problem is accentuated by the growing number of people, who eat irregularly and consume large portions of high-calorie food. For example, about 50% of the adult population in Europe with so-called disordered eating suffer from obesity.

The possible effects of this problem include physical health problems and loss of productivity. First of all, obesity results in incorrect functioning of the human body and contributes to the risk of developing some chronic illnesses. For example, as body fat percentage increases, the person’s metabolism worsens, which in turn may result in diabetes or heart diseases. Secondly, overweight people are very unhealthy and often suffer from stress and tiredness. This lessens their work capacity and results in lower productivity. For example, it has been proven that an obese person needs to put more effort to complete some task than a person with normal weight.

To sum up, obesity is a big problem that affects a lot of people nowadays. It’s mainly caused by inactive lifestyle and eating disorders and results in severe health problems and loss of productivity.

(251 words)

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Writing a cause and effect essay seems complicated and overwhelming, especially if you're unsure about where to start or how to structure your essay.

You might feel stuck, staring at a blank page, or confused by all the rules and guidelines. It's frustrating not to have clear examples and easy explanations to guide you through the process.

But don't worry!

In this blog, we will break down the complexities of cause and effect essays into simple, understandable steps. We will provide clear examples and straightforward tips, making essay writing easy. 

Let's read on.

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• 1. What is a Cause and Effect Essay 
• 2. Cause And Effect Essay Structure 
• 3. How To Write A Cause And Effect Essay 
• 4. Cause and Effect Essay Format
• 5. Cause And Effect Essay Examples 
• 6. Cause And Effect Essay Topics 
• 7. Tips for Writing Cause and Effect Essays

What is a Cause and Effect Essay 

According to cause and effect essay definition:

It is a type of academic writing that explores the reasons behind an event or situation (the cause) and the outcomes or consequences that result from it (the effect). 

In this essay, you have to dig deeper into the "why" and "what happens next" aspects of a particular topic.

Understanding Causes and Effects 

Consider the below questions to evaluate the effectiveness of a cause and effect essay:

• What are the causes and effects?
• What elements should be emphasized?
• Are there single or multiple effects and causes?
• How to list causes and effects in an essay?

The Purpose of a Cause and Effect Essay 

The primary goal of writing a cause and effect essay is to provide insights into how different elements relate to one another. It helps readers comprehend the underlying reasons for certain events or phenomena. It enables you to:

• Uncover Connections: Explore and explain the links between causes and their effects.
• Analyze Events: Break down complex events into manageable parts.
• Illustrate Patterns: Highlight recurring patterns and trends in various situations.

Cause And Effect Essay Structure 

A well-structured cause and effect essay outline is crucial for effectively conveying your ideas and insights. 

Here's how to craft an organized and compelling cause and effect essay:

How To Write A Cause And Effect Essay 

Writing a cause and effect essay can be a rewarding experience, allowing you to explore the relationships between events and their consequences. 

To help you craft an effective cause and effect essay, here is a step-by-step guide:

Step 1: Choose the Essay Topic 

Begin by choosing a topic that has significance and relevance. Look for subjects with clear cause-and-effect relationships to ensure your essay has a solid foundation. 

Consider both personal interests and the potential appeal to your target audience.

Step 2: Conduct Thorough Research 

Research is a fundamental step. Gather reliable information, data, and examples related to your chosen topic. 

Understanding the causes and effects comprehensively is vital for crafting a well-informed and persuasive essay.

Step 3: Create a Strong Thesis 

Your thesis statement is the core of your essay. It should clearly state whether you are focusing on causes, effects, or both. 

A well-crafted thesis provides direction for your essay and helps readers understand your essay's purpose.

Step 4: Structure Your Essay with an Outline 

An outline serves as a roadmap for your essay. It should detail the introduction, body paragraphs, and conclusion. 

Each paragraph should have a specific focus on a single cause or effect, ensuring a logical and organized flow.

Step 5: Craft Engaging Introduction 

The cause and effect essay introduction is your first impression. Use a compelling hook to capture the reader's attention. 

Provide necessary background information to help your audience understand the context. 

Clearly state your thesis to set the stage for what's to come in your essay.

Step 6: Develop Detailed Body Paragraphs 

The body of your essay is where you explore causes and effects in depth. Each paragraph should start with a topic sentence that introduces a specific cause or effect. 

Provide detailed explanations, supporting evidence, and illustrative examples to back your points. 

Use smooth transitions to maintain a coherent flow between paragraphs.

Step 7: Address Counter Arguments in the Antithesis Paragraph 

To present a well-rounded perspective, include an antithesis paragraph. This section allows you to acknowledge opposing viewpoints related to your topic. 

By addressing counter arguments, your essay becomes more comprehensive and persuasive.

Step 8: Write an Effective Conclusion 

The conclusion should wrap up your essay effectively. Restate your thesis statement for cause and effect essay to remind readers of your main argument. 

Summarize the key insights discussed throughout your essay. 

Conclude with a thought-provoking sentence that leaves a lasting impression on your audience.

Cause and Effect Essay Format

In addition to structuring your cause and effect essay effectively, adhering to formatting guidelines is essential.

Here are the key formatting guidelines to follow:

• Font Type: Opt for widely accepted fonts such as Times New Roman or Arial. These fonts are easy to read and maintain consistency in your document.
• Font Size: Keep the text within your essay at a 12-point font size. This standard size ensures that your content is legible and easily comprehensible.
• Line Spacing : You have two choices for line spacing: either 1.5 or double line spacing. Double spacing may be more suitable for lengthy essays, while 1.5 spacing strikes a balance between readability and conservation of space.
• Alignment: Align your text to justify, which means both the left and right margins are straight. This creates a clean and organized appearance for your essay, enhancing its overall professionalism.
• Margins: Maintain one-inch margins on all sides of the document to give your essay a neat and well-structured look.

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Cause And Effect Essay Examples 

To gain a better understanding of how cause and effect essays are structured and written, it's often helpful to explore examples of cause and effect essays. 

Here are a few cause and effect essay pdfs that you can use as a starting point to guide your writing:

Cause And Effect Essay Sample

Cause And Effect Essay On Global Warming

Cause And Effect Essay On Climate Change

Covid 19 Cause And Effect Essay

Social Media Cause And Effect Essay

Poverty Cause And Effect Essay

Air Pollution Cause And Effect Essay

Cause And Effect Essay Examples College

Looking for more examples? Check out this cause and effect essay examples blog!

Cause And Effect Essay Topics 

Selecting the right topic is the foundation of a compelling cause and effect essay.. Here's a collection of thought-provoking topics that can serve as a great starting point for your essay:

• The Causes and Effects of Bullying on Mental Health
• The Impact of Divorce on Children
• The Causes and Effects of Global Warming on Human Health
• The Long term Effects of Peer Pressure on Decision-Making
• The Causes of Stress in the Modern World
• The Impact of Online Shopping on Traditional Retail
• The Causes and Effects of Immigration
• The Causes and Effects of Teenage Rebellion
• The Impact of Cell Phones on Personal Relationships
• The Causes and Effects of Political Polarization

Need more topics? Read our cause and effect essay topics blog!

Tips for Writing Cause and Effect Essays

Crafting a compelling cause and effect essay requires a thoughtful approach. Here are some valuable tips to help you excel in your essay writing process:

• Hook Your Readers: Begin with a compelling hook in your introduction to engage your audience from the start.
• Provide Detailed Explanations: In your body paragraphs, offer detailed explanations, supporting evidence, and examples for causes and effects.
• Use Transitional Phrases: Employ transitional words and phrases to ensure a smooth and logical flow between ideas.
• Consider Opposing Views: Include an antithesis paragraph to acknowledge contrasting viewpoints on your chosen topic.
• Tailor to Your Audience: Think about your target readers and adapt your language and examples to their understanding and interest levels.
• Avoid Plagiarism: Properly cite and reference all sources to maintain academic integrity and prevent plagiarism.
• Maintain Objectivity: Keep an objective tone throughout your essay, focusing on presenting well-supported causes and effects rather than personal opinions.
• Revise for Clarity: Review your essay to ensure that your cause-and-effect relationships are effectively and clearly conveyed.

All in all, this complete guide, examples, and tips will surely help you learn how to write a cause and effect essay step by step. Moreover, it will also refine your skills to get a better grade.

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Cause and Effect Essay - English - 30 Multiple Choice, Answers - 8th grades, 11 pages

Subject: English

Age range: 11-14

Resource type: Worksheet/Activity

Last updated

29 August 2024

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Welcome, 8th graders and higher grades, to an exciting journey into the world of writing! In this activity, we’ll explore the art of crafting a “Cause and Effect Essay” , which is a type of writing that allows you to investigate and explain the reasons behind events or actions and their subsequent consequences.

Why do certain things happen, and what happens because of them? That’s what this 11 page activity is all about—discovering the connections and patterns in our world in one hour.

During this 30 Multiple Choice activity, you will learn the essential elements of a Cause and Effect Essay, how to structure it effectively, and how to use transitional words to guide your readers through the causal relationships. You’ll also explore common mistakes to avoid and techniques to make your essay compelling and insightful thanks to the Answers included.

By the end of this English activity, you’ll be well-equipped to write your own Cause and Effect Essays and impress your teachers with your writing skills. Let’s dive in!

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• Published: 03 September 2024

Association between blood heavy metal element and all-cause mortality in asthmatic adults: a cohort study

• Jiaxin Liao 1   na1 ,
• Jun Wen 1   na1 ,
• Chengcheng Wei 2 , 3   na1 ,
• Rongjuan Zhuang 1   na1 ,
• Mohan Giri 1 &
• Shuliang Guo 1  

Scientific Reports volume  14 , Article number:  20457 ( 2024 ) Cite this article

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• Medical research

Asthma start, development, and exacerbation have all been linked in numerous studies to exposure to a variety of metal elements. However, there is still a dearth of epidemiological data linking heavy metal exposure to death in asthmatics. The investigation included 2432 eligible adults with asthma. The study examined the possible correlation between blood heavy metal levels and all-cause mortality. This was done by utilizing Cox proportional hazards models, restricted cubic spline (RCS), threshold effect models, and CoxBoost models. Subgroup analyses were conducted to investigate the associations between blood metal levels and all-cause mortality among distinct asthmatic populations. An inverse association was found between blood selenium and all-cause mortality in asthmatics, while blood manganese showed a positive association with all-cause mortality. However, there were no significant connections found between blood lead, cadmium, mercury, and all-cause mortality via multivariate Cox proportional hazard models. In model 3, after accounting for all factors, all-cause mortality dropped by 10% for every additional 10 units of blood selenium (μg/L) and increased by 6% for every additional unit of blood manganese (μg/L). The RCS and threshold effect model found a U-shaped correlation between blood selenium, blood manganese, and all-cause mortality. The lowest all-cause mortality among asthmatics was observed when blood selenium and manganese were 188.66 μg/L and 8.47 μg/L, respectively. Our investigation found a U-shaped correlation between blood selenium levels, blood manganese levels, and all-cause mortality in asthmatic populations. Optimizing dietary selenium intake and effectively managing manganese exposure could potentially improve the prognosis of asthma.

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Introduction.

Asthma is characterized by sporadic and diverse symptoms (such as difficulty breathing, chest constriction, wheezing, coughing, and production of phlegm) caused by bronchospasm and inflammation of the airways 1 . Currently, the global prevalence of this condition exceeds 350 million individuals, and it has been steadily increasing over the past few decades. Moreover, it is directly accountable for causing around 250,000 annual fatalities due to asthma 2 , 3 . Although most patients can be effectively treated, a considerable number of individuals with asthma fail to attain long-term control, resulting in a substantial economic burden. According to research, it is projected that the United States will experience economic losses of 963 billion dollars due to adult asthma in the next 20 years 4 .

The incidence and mortality rates of asthma are significantly linked to poverty and its related factors, which encompass limited access to healthcare and exposure to environmental elements such as allergens, tobacco smoke, air pollution, and a lack of beneficial microbial exposure 5 . Heavy metals are extensively utilized and distributed in the environment, and they can enter animal, human, and plant cells by being consumed by food, water, or air intake 6 . Lead, cadmium, mercury, and manganese are heavy metals found in polluted environments. These metals can enter the lungs and bloodstream through inhalation and ingestion. They can act individually or in combination to affect biological processes, including inflammation and oxidative stress pathways. These processes contribute to lung damage, such as asthma, and result in the premature deaths of millions of people annually 7 , 8 , 9 , 10 , 11 , 12 .

Lead is a significant air pollutant that directly disrupts the immune system and triggers an elevation in inflammatory mediators inside the body. This, in turn, results in the development of allergic asthma 13 . Empirical investigations have demonstrated that inhaling lead causes an elevation in IgE and histamine levels in animals that have been sensitized. Additionally, it leads to an increase in inflammatory indicators such as the total count of white blood cells, and exacerbates the severity of asthma, both during the advancement of the disease and after its symptoms have become apparent 14 . Our prior research indicates that long-term exposure to lead may be linked to immune system abnormalities in adults with asthma and can affect the onset, progression, and worsening of asthma 15 . An investigation conducted in the United States revealed that adult individuals who smoke have an elevated susceptibility to wheeze and asthma following exposure to elevated levels of cadmium. Additionally, exposure to cadmium or lead adversely impacts lung function in non-smoking adults 16 . Furthermore, scientific literature has documented a correlation between levels of mercury in the blood and the likelihood of school-aged children acquiring asthma. This link also impacts several aspects of asthma, including wheezing, the use of asthma medication, and respiratory hyperresponsiveness 17 . Experimental findings indicate that manganese exhibits cytotoxicity towards bronchial epithelial cells (BEAS-2B) when cultivated in vitro at various doses. This leads to the release of interleukins, which serve to attract immune system cells 18 . Nevertheless, certain investigations have indicated that optimal levels of manganese can mitigate, to some extent, specific asthma symptoms 19 .

Asthma has been linked to both environmental contaminants and deficiencies in micronutrients. Selenium is a micronutrient that has a multifaceted relationship with asthma. It is connected not only to the connection between selenium levels, glutathione peroxidase (GPX) activity, and oxidative stress but also to the balance between Th1 and Th2 immune responses 20 . Research has indicated that low levels of selenium in the overall population are linked to an increased likelihood of developing asthma. Additionally, supplementing with selenium has been found to enhance lung function in individuals with asthma 21 , 22 , 23 .

Current research has yielded, there have been limited studies that have specifically investigated the impact of various types of heavy metal exposure on the overall mortality rate in adult patients with asthma. This study utilized data from the National Health and Nutrition Examination Survey (NHANES) conducted between 2011 and 2018. We established specific criteria to select asthmatic individuals who met the requirements of the study and examined the relationship between certain elements (lead, cadmium, mercury, manganese, and selenium) and all-cause mortality in adults with asthma. We conducted a thorough investigation to determine if this correlation varies among different populations.

Materials and methods

Study data and population.

The Centers for Disease Control and Prevention (CDC) carried out the NHANES, a vital scientific endeavor that methodically evaluates the health and nutritional condition of both American adults and children. The CDC, responsible for supplying extensive health statistics for the country, has received official permission for NHANES methodology from the Research Ethics Review Board of the National Center for Health Statistics (NCHS). NHANES guaranteed participant rights by obtaining informed written consent from all individuals who participated in the study. All methods in this study were carried out in accordance with relevant guidelines/regulations. The data we collected from NHANES covered the time frame between 2011 and 2018. Figure 1 illustrates that NHANES had a participation of 39,156 people from 2011 to 2018. Adhering to specific inclusion and exclusion criteria, our study population excluded: (1) individuals under 18 years old (n = 15,331); (2) individuals without asthma or with missing data (n = 20,213); (3) those lacking blood heavy metal data (n = 1174); (4) those with missing follow-up data (n = 6). Finally, our investigation involved a huge sample of 2432 asthmatic adults in the USA.

Flow diagram delineating the participant selection protocol for the investigated cohort.

Measurement of blood metal

The exposures of whole-blood lead (Pb), cadmium (Cd), mercury (Hg), selenium (Se), and manganese (Mn) were measured using inductively coupled plasma-dynamic reaction mass spectrometry (ICP-DRC-MS) on either an ELAN 6100 DRC Plus or ELAN DRC II instrument (PerkinElmer Instruments, Headquarters Office, 710 Bridgeport Ave., Shelton, CT 06,484–4794) at the CDC’s National Center for Environmental Health. Concentrations that were too low to be detected (below the limit of detection, LOD) were estimated by using the value of LOD divided by the square root. Detailed information about laboratory quality assurance and monitoring can be found on the NHANES website.

Assessment of mortality

We employed unique study identifiers and performed probabilistic matching with the National Death Index (NDI) as of December 31, 2018, to ascertain the vital status of our participants. The NCHS provided additional information on the matching methodology. In addition, we used the 10th edition of the International Statistical Classification of Diseases (ICD) ten to determine mortality status. We primarily focused on all-cause mortality.

In order to address the potential confounding effects of diverse factors, we incorporated numerous covariates into our investigation. The covariates considered in the analysis were gender (male and female), age, ethnicity (non-Hispanic white, non-Hispanic black, other race), levels of education (less than high school, high school, more than high school), poverty-to-income ratio (PIR), status in marriage (married, single, living with a partner), body mass index (BMI), smoking status (smoker: individuals with a history of smoking over 100 cigarettes; non-smoker: individuals with a history of smoking less than 100 cigarettes), intake of alcohol, serum cotinine, hypertension history (Yes, No), diabetes history (Yes, No), cardiovascular disease (CVD) history (Yes, No), chronic obstructive pulmonary disease (COPD) history (Yes, No), malignancy history (Yes, No), alanine aminotransferase (ALT), aspartate aminotransferase (AST), serum creatinine, and urine creatinine. Asthma status was ascertained using standardized questionnaires presented during participants’ visits, employing the query, "Have you ever been diagnosed with asthma by a physician or other healthcare professional?" Participants who answered positively were classified as having a diagnosis of asthma. Participants’ CVD was verified based on self-reported physician diagnoses obtained through individual interviews using a standardized questionnaire to evaluate medical conditions. The participants were queried about whether they had ever received information from a physician or other healthcare professional regarding their diagnosis of congestive heart failure, coronary heart disease, angina pectoris, heart attack, or stroke. An affirmative answer to any of these items categorized an individual as having CVD.

Statistical analysis

Statistical analyses were performed utilizing R software (version 4.2.0). A significance threshold of p  < 0.05 was established. In order to tackle the intricate sampling design of the NHANES, sample weights were implemented. Utilizing the chi-square test for categorical variables and the Kruskal–Wallis test for continuous variables, baseline characteristics among groups were compared according to survival outcome. In the beginning, we developed three Cox proportional hazards regression models to assess the independent association between each blood heavy metal and all-cause mortality in individuals with asthma, while also accounting for numerous covariates. Following this, metals that demonstrated statistical significance were chosen for analysis using trend tests and Cox regression. Multiple imputation was used to handle variables with missing values, ensuring that the total proportion of missing values for each covariate was less than 10%. In order to investigate the association between blood heavy metals and all-cause mortality, we utilized restricted cubic splines (RCS) and a threshold effect model to assess both linear and non-linear relationships. When dealing with a nonlinear connection, the inflection point was identified by methodically evaluating all potential values and choosing the inflection point with the greatest probability. Subsequently, a two-piecewise Cox proportional risk model was utilized to examine the association between blood metals and the probability of all-cause death, separately on each side of the inflection point. Stratified studies were performed to investigate the correlation between blood metals and overall mortality in various groups of people with asthma. Finally, the CoxBoost algorithm model was employed to thoroughly assess the relative impact of each metal on the status of survival.

Ethical approval and consent to participate

Before implementing the data collection techniques and conducting thorough health examinations, all participants finished informed consent voluntarily. The NHANES study protocol received approval from the Research Ethics Review Board of the NCHS (Ethical approval number: Protocol #2011-17, Protocol #2018-01).

Baseline characteristics based on survival status of study individuals

Provided in Table 1 were the baseline characteristics of people involved in the cohort study (N = 2432), grouped according to their survival outcomes. The individuals with asthma under analysis displayed an average age of 45.91 years, with 57.46% being female. The median period of follow-up for all asthmatics was 57.89 months. Significant variations were observed in the distributions of age, educational level, PIR, smoking status, history of hypertension, diabetes, CVD, COPD and malignancy, serum creatinine, blood lead, and blood cadmium among different survival outcome groups. A comparison between individuals who deceased and those who survived revealed that the former were more likely to be elderly, have a lower education level, possess a reduced PIR, engage in smoking, have a history of hypertension, diabetes, CVD, COPD, and malignancy, and exhibit elevated levels of serum creatinine, blood lead, and blood cadmium.

Association between blood metals and all-cause mortality

The analysis of both univariate and multivariate Cox proportional hazard models (Table 2 ) revealed a significant inverse connection between blood selenium levels and all-cause mortality in individuals with asthma. However, the levels of manganese in the blood showed a significant positive relationship only with all-cause mortality when analyzed using multivariate Cox proportional hazard models (models 2 and 3). Significantly, there were no apparent connections between blood lead, cadmium, mercury, and all-cause mortality in model 3. In model 3, after accounting for various factors such as sex, age, race, education, marital status, and more, it was found that all-cause mortality decreased by 10% for every additional 10 units of blood selenium (μg/L). Conversely, the all-cause mortality increased by 6% for every additional unit of blood manganese (μg/L). In addition, the trend test (Table 3 ) indicated a potential linear correlation between blood selenium and all-cause mortality in model 3 ( p for trend < 0.05), while suggesting a potential non-linear correlation between blood manganese and all-cause mortality in model 3 ( p for trend > 0.05). Besides, we found no significant correlation between blood selenium, lead, cadmium, mercury, manganese levels and respiratory disease-related mortality in multivariate Cox proportional hazards regression models (Supplementary Table 1 ).

Restricted cubic splines (RCS) and threshold effect model

Our investigation utilized RCS and a threshold effect model to investigate the association between blood selenium, blood manganese, and all-cause mortality in persons with asthma. The objective was to ascertain whether the relationships were linear. The analysis, including all covariates, showed a U-shaped relationship between blood selenium, blood manganese, and all-cause mortality(Figures 2 A,B). The non-linearity and overall p -values were both below 0.05, demonstrating a non-linear association between blood selenium, blood manganese, and all-cause mortality. Following that, a threshold effect analysis was performed to determine the points of inflection. The inflection points for blood selenium and manganese were determined as 188.66 and 8.47, respectively, based on log-likelihood ratio p -values that were less than 0.05. These inflection points corresponded to the lowest all-cause mortality among asthmatics. Table 4 demonstrates significant disparities between model A (the single-line model) and model B (the segmented regression model). The segmented regression model provided a more reasonable explanation for the non-linear association between blood manganese, selenium, and all-cause mortality in persons with asthma.

Association between blood selenium (A), blood manganese (A), and all-cause mortality in asthmatic adults. The red solid line and red area correspond to the HR and their corresponding 95%CI, separately.

Subgroup analysis

Subgroup analyses were carried out to evaluate the links between blood selenium, blood manganese, and all-cause mortality in various asthmatic populations. The outcomes, grouped by gender, age, race, BMI, history of hypertension, diabetes, CVD, COPD, and malignancy, appeared in Table 5 . A negative link was shown between blood selenium levels and all-cause mortality in asthmatic adults over the age of 60 who were non-Hispanic white, had a BMI below 30, and did not have hypertension or malignancy. In addition, those with asthma who had high levels of manganese in their blood, especially females, individuals of other race, those with hypertension and CVD, and those without a history of COPD or malignancy, had a higher risk of mortality from all-cause compared to those with lower levels of blood manganese.

The relative effect of each variable by the CoxBoost model

To assess the relative impact of each blood metal level on the survival status of the study population, we employed the CoxBoost algorithm model. This model evaluated the positive and negative effects of blood lead, cadmium, mercury, selenium, and manganese on the risk of all-cause mortality in asthmatics. The results of the CoxBoost model, illustrated in Figure 3 , revealed that blood metals with a positive impact on mortality risk, in descending order of effect size, were lead and cadmium. Conversely, blood metals associated with a decreased risk of death, in descending order of effect size, were selenium. Due to its minimal effect, manganese was not visually represented in Figure 3 . Among the selected metals, selenium exhibited the most substantial impact on the survival status of individuals with asthma.

The CoxBoost model assessed the positive and negative effects of each blood metal level in relation to the survival outcome of the follow-up.

Heavy metal contamination is a highly significant environmental issue in the modern world. As humans occupy the highest position in the food chain, they will unavoidably consume different types of heavy metals as a result of the bioconcentration effect 24 . Asthma is a prevalent chronic respiratory condition characterized by persistent inflammation of the airways and increased sensitivity to various stimuli from many sources 25 , 26 . Several studies have indicated an association between the exposure to specific heavy metal ions and the occurrence of asthma. In a meta-analysis of children’s hypersensitivity diseases, Wang et al. discovered a correlation between copper exposure and childhood asthma 27 . Similarly, Miyazaki et al. 28 observed that exposure to mercury and manganese during pregnancy heightened the likelihood of asthma in early childhood. Furthermore, there exists a link between the presence of heavy metals and the likelihood of developing active asthma. Wu et al. discovered a favorable correlation between elevated levels of mercury and lead in the bloodstream and the occurrence of wheezing events in children diagnosed with asthma 29 . Patients afflicted with asthma face an elevated risk of mortality. Osvald et al. observed a noteworthy rise in overall mortality among individuals with asthma compared to those without the condition, particularly among children and young people 30 . Nevertheless, there is limited research on the association between exposure to heavy metals and mortality in individuals with asthma. Therefore, we undertook this study to investigate whether heavy metal exposure acts as a contributing factor to the risk of death in asthma patients.

A total of 2432 participants who had asthma were assessed for the study based on predetermined exclusion criteria. We documented the correlation between blood metal concentrations and all-cause mortality in adult asthmatics by examining their blood concentrations of selenium, various metal elements, and related clinical indicators. After adjusting for multiple variables, our study found that blood manganese levels were significantly positively correlated with all-cause mortality in asthmatics. However, univariate analysis and analysis adjusted for certain variables suggested that blood lead and blood mercury levels might be related to mortality in asthma patients. Both univariate and multivariate analyses revealed a negative connection between blood selenium level and all-cause mortality in asthma patients. It was inaccurate to conclude, however, that a longer life for asthma was associated with lower blood manganese levels and higher blood selenium levels, based alone on these findings. We established nonlinear models of all-cause mortality and blood selenium or blood manganese, respectively, using restricted cubic splines. The results showed a U-shaped correlation: patients who had either a concentration too high or too low would have a higher risk of dying, while there was a certain concentration that reduced that risk, which was also supported by the threshold effect model.

One of the most important microelements in the human body, manganese is primarily needed as an enzyme cofactor for enzymes like manganese superoxide dismutase (Mn-SOD) and is present in a variety of metalloproteins 31 . One of the essential components of the mitochondrial antioxidant system, Mn-SOD, may generate superoxide radicals at a disproportionate rate and protect the mitochondria from damage brought on by a range of oxidants 32 . Furthermore, manganese contributes to the structure of the enzymes pyruvate carboxylase 33 , arginase 34 , and glutamine synthetase 35 . Low manganese levels have been linked to an increase in NO and a decrease in arginase activity, which increases airway responsiveness in asthmatic children 19 . On the other hand, an excessive buildup of manganese may also be detrimental to human health. Overdosing on manganese is considered cytotoxic and linked to several neurodegenerative illnesses 36 . Exposure to manganese may cause a pathological increase in the intracellular autophagic process, impairing cellular energy metabolism among other processes 37 . In asthmatics, metabolic anomalies like those brought on by high manganese concentrations can harm the airways and raise the chance of death.

Another one of the necessary microelements is selenium. Glutathione peroxidase 38 , iodothyronine deiodinase 39 , selenoprotein P 40 , and thioredoxin reductases 41 , among other selenoproteins, are examples of selenium’s functional forms. These enzymes are involved in the regulation of antioxidants, DNA synthesis, thyroid hormone metabolism, and numerous other biological processes. Research has revealed that blood selenium concentrations are lower in asthma sufferers than in healthy individuals 42 . Because it controls the activity of immune cells such T helper cells, selenium may have an impact on the development of asthma 22 . Significantly, a high selenium intake has toxicological consequences on the human body that harm the respiratory, digestive, and cardiovascular systems, among other organs 43 , 44 .

It is well known that heavy metals such as lead, cadmium, and mercury have an impact on human health 6 , 7 , 13 . However, this study found that certain heavy metal elements do not appear to be significantly associated with all-cause mortality in asthma patients. This may be because the effects of these elements are masked or balanced under the influence of multiple confounding factors, and the effects of these elements may require more complex mechanisms to explain. Selenium and manganese showed a significant correlation with all-cause mortality in asthma patients due to the impact on the overall health status of patients. However, the two and other elements such as lead, cadmium, and mercury were not significantly related to respiratory system-related mortality. This may be because these elements do not directly damage or act on the respiratory system and thus cannot effectively affect the incidence and severity of respiratory diseases.

Unlike other studies, ours focused on explaining the relationship—which had not been previously documented by other researchers—between blood heavy metal concentrations and all-cause mortality in asthmatics. After selecting the two elements with the highest correlation—manganese and selenium—we analyzed the remaining elements using Cox proportional hazard models. We discovered that asthma patients would have a higher risk of mortality if there were either excessively high or low amounts of the two components. This provides valuable insights for establishing specific reference levels for blood selenium and manganese concentrations in asthmatic patients, as well as helping these patients modify their dietary regimens and toxic exposure.

Our investigation does, however, still have certain shortcomings. First off, the majority of the study participants were asthmatics from the United States. Data from other nations still need to be further incorporated because there are regional variations in environmentally induced heavy metal exposure. Secondly, the medical care that the research participants received was not considered in the study. Third, a large number of confounding variables may still exist and may not have been taken into account. Unquestionably, systematic asthma treatment plays a significant role in enhancing asthma patients’ prognosis. Nonetheless, knowing the body’s levels of selenium, manganese, and other elements may help with more effective medical care. The prognosis of patients may be improved by maintaining certain levels of selenium and manganese through dietary adjustments and manganese exposure.

The investigation identified a U-shaped correlation between the levels of selenium and manganese in the blood of adult asthmatics and their risk of all-cause mortality. This discovery indicates that both excessive and insufficient levels of manganese and selenium have harmful effects on the longevity of patients with asthma. Our research contributes to the understanding of the relationship between levels of heavy metals in the blood and the risk of death in individuals with asthma. Moreover, our findings suggest that modifying the amount of selenium in the diet and managing exposure to manganese could potentially improve the prognosis for individuals with asthma.

Data availability

All accessible data is available on the official NHANES website ( http://www.cdc.gov/nchs/nhanes/index.htm ).

Abbreviations

National health and nutrition examination survey

Restricted cubic splines

National death index

Centers for disease control and prevention

National center for health statistics

Poverty to income ratio

Body mass index

Cardiovascular disease

Chronic obstructive pulmonary disease

International statistical classification of diseases

Confidence interval

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These authors contributed equally: Jiaxin Liao, Jun Wen, Chengcheng Wei and Rongjuan Zhuang.

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Department of Respiratory and Critical Care Medicine, The First Affiliated Hospital of Chongqing Medical University, Chongqing Medical University, Chongqing, China

Jiaxin Liao, Jun Wen, Rongjuan Zhuang, Mohan Giri & Shuliang Guo

Department of Urology, The First Affiliated Hospital of Chongqing Medical University, Chongqing Medical University, Chongqing, China

Chengcheng Wei

Department of Urology, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei, China

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J.W. participated in the study design, data extraction, statistical analysis, drafting and revision of the manuscript. J.X.L. performed the study design, statistical analysis, and drafted and revised the manuscript. C.C.W. conducted the study design and the data extraction, and revised the manuscript. R.J.Z. carried out statistical analysis and drafted the manuscript. M.G. carried out the data extraction and revised the manuscript. S.L.G. took part in the study design, management, and revision of the paper. All authors read and approved the final manuscript.

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Liao, J., Wen, J., Wei, C. et al. Association between blood heavy metal element and all-cause mortality in asthmatic adults: a cohort study. Sci Rep 14 , 20457 (2024). https://doi.org/10.1038/s41598-024-70250-8

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• Published: 04 September 2024

Divergent effects of tumor necrosis factor (TNF) in sepsis: a meta-analysis of experimental studies

• Christian Kassasseya 1 ,
• Ligia Iulia Torsin 2 , 3 ,
• Caroline Musset 1 ,
• Marc Benhamou 4 , 5 ,
• Irshad H. Chaudry 6 ,
• Jean-Marc Cavaillon 7 ,
• Nathalie Grall 8 ,
• Renato Monteiro 4 , 5 , 9 ,
• Luc de Chaisemartin 4 , 5 , 9 ,
• Dan Longrois 2 , 10 , 11 ,
• Philippe Montravers 2 , 12 &
• Christian de Tymowski 2 , 4 , 5 , 10  

Critical Care volume  28 , Article number:  293 ( 2024 ) Cite this article

Metrics details

Introduction

Experimental studies in animals have yielded conflicting results on the role of Tumor Necrosis Factor (TNF) in sepsis and endotoxemia, with some reporting adaptive and others inappropriate effects. A meta-analysis of the available literature was performed to determine the factors explaining this discrepancy.

The study followed the Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) statement. The protocol was registered with PROSPERO (CRD42020167384) prior to data collection. PubMed and Embase were the databases queried. Risk of bias was evaluated using the SYRCLE Risk of Bias Tool. All animal studies investigating sepsis-related mortality and modified TNF signaling were considered eligible. The exclusion criteria were: lack of mortality data, 7-day mortality rates below 10% in both wild type and TNF-altered pathway animals, and absence of an English abstract. To determine the role of TNF according to the experimental protocol, three approaches were used: first an approach based on the statistical significance of each experiment, then the pooled mortality was calculated, and finally the weighted risk ratio for mortality was assessed.

A total of 175 studies were included in the analysis, comprising a total of 760 experiments and involving 19,899 animals. The main species used were mice (77%) and rats (21%). The most common method of TNF pathway modulation was TNF pathway inactivation that was primarily associated with an inappropriate secretion of TNF. At the opposite, TNF injection was associated with an adaptive role of TNF. Lipopolysaccharide (LPS) injection was the most used stimulus to establish an infectious model (42%) and was strongly associated with an inappropriate role of TNF. Conversely, live bacterial models, especially the cecal ligation and puncture (CLP) model, pneumonia, meningitis, and gastrointestinal infection, were associated with an adaptive role. This was particularly evident for Listeria monocytogenes, Streptococcus pneumoniae .

The role of TNF during infection varies depending on the experimental model used. Models that mimic clinical conditions, based on virulent bacteria that cause high mortality even at low inocula, demonstrated an adaptive role of TNF. Conversely, models based on LPS or low-pathogenic live bacteria, administered at doses well above physiological thresholds and combined with early antibiotic therapy, were associated with an inappropriate role.

Graphical abstract

Ten years after its discovery in 1975 [ 1 ], early Tumor Necrosis Factor (TNF) secretion following injection of lipopolysaccharide (LPS) or live Escherichia coli was found to be associated with mortality in two studies conducted by Cerami’s team [ 2 , 3 ]. These articles opened a new perspective on sepsis by demonstrating the crucial role of inflammation in sepsis-related pathophysiology. Thus, sepsis-related mortality may depend on host-related factors, which explain the persistence of high mortality rates in sepsis despite the use of antibiotics. The initial human studies tended to support this hypothesis. Waage et al. reported the presence of circulating TNF in patients with sepsis and found a correlation between circulating TNF levels and mortality in meningococcal infections [ 4 ]. In addition, the injection of low doses of LPS resulted in the production of TNF and physiological changes commonly observed in sepsis, such as fever, tachycardia, and changes in cardiac output [ 5 ]. Furthermore, in 1993, a voluntary self-injection of high doses of LPS rapidly led to septic shock with very high levels of TNF [ 6 ]. As a result, blocking TNF secretion was considered a new strategy to reduce sepsis mortality. However, subsequent human studies have shown that blocking TNF secretion did not reduce sepsis mortality [ 7 , 8 , 9 , 10 ], and one study even found excess mortality after blocking TNF biological activity in sepsis [ 11 ]. One explanation for these failures is that TNF may also play an adaptive role in sepsis. In fact, as early as 1987, other experimental studies found an adaptive role for TNF in cecal ligation and puncture (CLP) and in listeriosis [ 12 , 13 ]. This led to the concept of cytokines as a double-edged sword in sepsis [ 14 , 15 ].

Therefore, almost 50 years after its discovery, the precise role of TNF secretion in sepsis remains controversial: is it an adaptive or inappropriate factor? We conducted a systematic literature review to investigate the factors that may account for the varying outcomes of TNF action in experimental studies. These factors include the animal species, infectious model and pathogens used, and the type of modulation of the TNF pathway.

Recommendations for conducting a systematic review

The study followed the Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) statement [ 16 ] (Online Appendix 1 ) and the recommendation of Cochrane Handbooks for meta-analysis [ 17 ].

Data retrieval strategies

The study protocol was registered in 2020 with PROSPERO (CRD42020167384) before data collection began. We searched in 2020 PubMed and Embase databases for articles containing TNF-evoking terms in their titles, combined with terms related to infections (such as peritonitis, pneumonia), names of specific bacteria (e.g., E. coli ), or references to endotoxin (LPS). The search equation in Embase was as follows: (‘tumor necrosis factor’:ti OR ‘TNF’:ti OR 'cachectin':ti OR ‘rTNF’:ti) and ('sepsis':ti OR 'septic shock':ti OR 'Gram-positive shock':ti OR 'Gram- negative shock':ti OR 'infection':ti OR 'infections':ti OR 'endotoxin':ti OR 'endotoxemia':ti OR 'pneumonitis':ti OR ‘peritonitis’:ti OR 'bacterial growth':ti OR ‘pneumoniae’:ti OR ‘pneumonia’:ti OR ‘aureus’:ti OR ‘coli’:ti OR ‘salmonella’:ti OR ‘pseudomonas’:ti OR 'caecal ligation and puncture':ti OR 'infectious':ti OR ‘listeria’:ti OR ‘listeriosis’:ti OR ‘pyogenes’:ti OR ‘lethality’:ti OR ‘endotoxic’:ti OR ‘pneumococcal’:ti OR ‘streptococcal’:ti OR ‘meningitis’:ti). The search equation for PubMed can be found in Online Appendix 2 . To ensure completeness, studies known to the authors that did not match the search equation but met the inclusion criteria were also included. Study eligibility criteria were assessed using the Covidence online software ( https://www.covidence.org/ ).

Two authors independently screened articles for inclusion based on their titles and abstracts. In case of disagreement, a third author intervened to resolve the issue. The third author was also responsible for including full-text articles. Data extraction was independently performed by the third and fourth authors.

Study eligibility criteria

All experimental studies were eligible, without time limitations. To be included in the analysis, studies had to fulfill all the inclusion criteria, and none of the exclusion criteria.

Inclusion criteria were: animal studies; investigation of mortality associated with sepsis, defined as an infection that causes mortality in less than 7 days; utilization of an infectious or infectious-like stimulus, including cecal ligation and puncture, injection of live bacteria or endotoxins, cutaneous infection, pneumopathy, peritonitis; modification of the TNF pathway in at least one group, encompassing any form of TNF inactivation (such as injection of anti-TNF antibodies, infusion of soluble TNF receptor, TNF knock-out animals, TNF receptor knock-out animals) or infusion of recombinant TNF.

Exclusion criteria were: human studies; reviews and meta-analyses; lack of mortality data; 7-day mortality rate below 10% in both wild type and TNF-altered pathway animals; absence of an English abstract; articles in languages that are not easily translated.

The 10% mortality cut-off for defining sepsis was based on the Sepsis III definitions [ 18 ].

Data collection

The following data were collected:

Publication-related data: first author's name, journal title, and publication year.

Experimental protocol-related data: type of TNF pathway modulation (inactivation or recombinant TNF infusion), method of TNF pathway inactivation (monoclonal or polyclonal antibody injection, soluble receptor injection, TNF or its receptors, knock-out mice), and co-injection of antibiotics.

Animal-related data: species, age, and sex of the animals

Statistical data for each experiment: number of animals used, number of events by arm (control vs. TNF pathway modulation) and, if available, the p-value and the test used to assess the significance of the difference in mortality.

Statistics on included articles

If a study included as least one mortality experiment, all experiments were included in the analysis. The log-rank test was considered the gold standard for assessing mortality, and this test was preferred. If mortality statistics were missing, but mortality data were available, mortality statistics were performed using GraphPad Prism version 6.00 for Windows, GraphPad Software, La Jolla, California, USA . A log-rank test was performed when available data allowed, otherwise a Fisher test was used. In addition, if a Fisher test was performed in the publication, but the data allowed for a log-rank test, the latter was performed and considered the primary statistical test to determine the role of TNF. A p-value of 0.05 was used to determine the statistical significance.

Definitions

Encapsulated bacteria were those known to possess an extracellular polysaccharide capsule, such as Klebsiella pneumoniae , Salmonella species, Streptococcus pneumoniae , and, when explicitly specified, Escherichia coli (strain 018: K1: H7) and Staphylococcus aureus (strain ATCC 25923, strain S 834). Parasitic infections were defined as those caused by eukaryotic organisms. Experiments (not studies) were classified into three groups according to the mortality observed and the p value of the statistic test used to determine the significance of the difference in mortality:

“Inappropriate" effect of TNF: if the mortality rate of control mice was statistically lower than that of mice in which the TNF pathway had been enhanced, or if the mortality rate of control mice was statistically higher than that of mice in which the TNF pathway had been decreased/blocked/inactivated/absent.

“non-significant" effect of TNF: if the mortality rate of control mice was not statistically different from that of mice in which the TNF pathway had been modified.

“Adaptive" effect of TNF: if the mortality rate of control mice was statistically higher than that of mice in which the TNF pathway had been enhanced, or if the mortality rate of control mice was statistically lower than that of mice in which the TNF pathway had been decreased/blocked.

A study was considered to show discordance in the role of TNF if it included experiments demonstrating both an inappropriate and an adaptive effect.

Assessing the risk of bias

Risk of bias was assessed using the SYRCLE Risk of Bias Tool [ 19 ]. This tool is an adaptation of the Cochrane Collaboration Risk of Bias Tool for use in animal studies. Of the ten possible biases, nine are well identified and the tenth corresponds to the other possible biases. In this study, this 10th bias included three items: lack of mortality statistics, the justification of the initial inoculum, and the presence of bacteriological and cytokine analyses. A bias was retained if it was present for at least one outcome of an experiment. Further details regarding the implementation of bias management strategies can be found in Online Appendix 3 .

Deviations from the initial protocol

Two modifications were made to the initial protocol during the study to enhance its quality. Firstly, additional terms were integrated into the equation search to maximize the number of studies included. This was implemented three months after the study commenced, during the screening process (Online Appendix 4 ). Secondly, a random-effects meta-analysis was included in the statistical analysis to consider the heterogeneity of the included experiments more effectively.

Systematic review and meta -analysis statistics

To produce this systematic review statistics, all experiments were grouped together in a single database (no statistic was performed at the study level). Three distinct methodologies were employed to determine the role of TNF in accordance with the experimental protocol.

Firstly, an approach based on the statistical significance of each experiment was employed. Univariate analysis compared the three roles of TNF: inappropriate, non-significant and adaptive. Categorical variables were expressed as numbers and percentages and were compared using the Chi-square test. Quantitative variables were expressed as median and interquartile range [25–75] and were compared by the Mann–Whitney U test or Kruskal–Wallis test as appropriate. To identify the independent factor associated with the effect of TNF, the adaptive and inappropriate roles were evaluated in a multivariate analysis using a binary logistic regression model. For both models, variables with nominal two-tailed p values below 0.1 were included in the multivariate model. The final models were selected using the backward stepwise regression method using the AIC and by excluding all significant variables with clear collinearity or with a variance inflation factor (VIF) superior to 5 [ 20 ].

Two approaches were then employed based on the raw data. Firstly, overall mortality rates were calculated by summing the number of deceased and surviving animals in each experiment, categorized by infection type and pathogen, and compared using the Mann–Whitney U test. Finally, a meta-analysis was conducted, to calculate the weighted risk ratio of mortality. Considering the significant heterogeneity between studies, the Mantel–Haenszel approach in a random-effects model was used to determine the weighted risk ratio for mortality [ 17 ].

All statistical analyses were performed using R software (R Core Team, 2014). Figures were generated using the ‘ggplot2 package’, and the meta-analysis was performed using the ‘meta package’. A p value < 0.05 was considered statistically significant.

A total of 4190 distinct studies were identified through keyword searches of the Embase and PubMed databases and screened based on titles and abstracts. Of these, 261 studies were identified as potentially relevant and were further screened for eligibility based on their full text. Ultimately, 164 studies were included using this method. In addition, 11 studies that met the inclusion criteria but were not captured by the keyword searches were subsequently included. In total, 175 studies were included in the meta-analysis (Fig.  1 and Online Appendix 5 ). Ten eligible publications were not included, due to unavailable data, including three written in Chinese with no available translation. The publication dates of the articles span 34 years, from 1985 to 2019.

These publications represent a total of 760 experiments, with a median of 3 [2–7] experiments per article, and a total of 19,899 animals, with a median of 22 [16–37] animals per experiment. A non-significant secretion was the main effect observed in 310 (41%) experiments, while an inappropriate role was observed in 261 (34%) experiments and an adaptive role in 189 (25%) experiments.

Influence of the animal species and of the genetic background

Most experiments were performed in mice (583, 77%) and rats (157, 21%). Rarely, experiments were performed in non-human primates (0.9%), rabbits (0.8%) or pigs (0.9%) (Table  1 ). Overall, most experiments (41%) were inconclusive regarding a clear role of TNF, while the majority of conclusive experiments favored an inappropriate role. However, careful analysis revealed subtle differences between species. Indeed, experiments showing an adaptive effect of TNF were more frequently seen in mice (28% of mouse experiments) than in rats (16% of rat experiments). In rabbits, pigs, and non-human primates, TNF was associated with an inappropriate role in more than half of the experiments, without any adaptive role.

The genetic backgrounds of mice were mainly C57BL/6 (236 out of 583 experiments, 40%), BALB/C (112, 19%) and Swiss (54, 9.3%) (Supplemental Table 1). In the subgroup analyses, a significant proportion of the mice experiments (ranging from 50% for Swiss mice to 31% for C3H mice) demonstrated a non-significant effect of TNF. The analyses of the conclusive experiments showed clear differences between the mice strains. The ratio of experiments concluding to an inappropriate effect to those concluding to an adaptive effect was 1.19 for C57BL/6 mice, 5.54 for BALB/C and 0.28 for Swiss mice, showing that experiments in BALB/C mice were more often associated with an inappropriate role of TNF, whereas experiments in Swiss mice were mainly associated with an adaptive role. Furthermore, mice aged between 8 and 12 weeks were more often protected by TNF, whereas no clear difference was observed between the sexes.

Influence of the type of modulation of the TNF signaling pathway

Modulation of the TNF pathway was achieved more frequently by its inactivation (604 out of 760 experiments, 79%) than by its stimulation (156 experiments, 21%) (Table  2 ). Stimulation of the TNF pathway was mainly achieved by injection of recombinant TNF (140 out of 156 experiments, 90%). The type of modulation was strongly associated with the observed effect (Fig.  2 ). Stimulation of the TNF pathway, specifically by injection of recombinant TNF, was associated with an adaptive role in half of these studies (73 out of 140, 52%, p  < 0.001). It should be noted that in the studies where recombinant TNF was injected, TNF was often found to be inappropriate when administered after infection (4 out of 7, 57%), whereas it was often found to be adaptive when administered before infection (60 out of 73, 82%). In contrast to the activation of the TNF pathway, the experiments with its inactivation led to the conclusion of an inappropriate role of TNF in 250 out of 604 experiments (41%), an undetermined role in 246 experiments (41%), and an adaptive role of TNF in 108 experiments (18%) (Table  2 and Fig.  2 ). However, a separate analysis of these experiments revealed a more complex picture. Experiments with knock-out (KO) mice for TNF pathways had a higher proportion of adaptive than inappropriate roles for TNF, 47 (32%) and 39 (26%) of 147 experiments, respectively ( p  = 0.029). Conversely, injection of anti-TNF antibodies or especially soluble TNF receptor, was strongly associated with an inappropriate role of TNF, especially when TNF inactivation occurred before or concomitantly with infection.

Animal mortality according to the type of TNF pathway modulation. Box plot of mortality by experiments, compared using the Mann–Whitney U test. Number of animals: A: control = 2758, TNF stimulation = 2302; B: control = 7802, TNF Inactivation = 7049.

Influence of the sepsis model

Analysis of the conclusive experiments reveals that animal models of peritonitis (CLP), pneumonia, and meningitis were associated with an adaptive role of TNF, whereas intraperitoneal injection of feces or bacteria, and intravenous injection of pathogen (the most used model; 39% of experiments), were strongly associated with an inappropriate role (Table  3 and Fig.  3 ). Mice in models demonstrating an inappropriate role of TNF had a mortality rate ≥ 90% earlier than those showing an adaptive role, respectively 2 days [1–3] versus 4 days [3–5] ( p  < 0.001).

Animal mortality according to the model of sepsis, with TNF pathway inactivation. Box plot of mortality by experiments, compared using the Mann–Whitney U test. Number of animals: Intravenous injection: control = 3388, TNF inactivation = 2989; Intraperitoneal injection: control = 2424, TNF inactivation = 2224; Caecal ligation and puncture: control = 1030, TNF inactivation = 877; Pneumonia: control = 460, TNF inactivation = 444; Skin infection: control = 199, TNF inactivation = 199; Meningitis: control = 135, TNF inactivation = 144; Gastro-intestinal infection: control = 160, TNF inactivation = 166

Influence of the type of infectious stimuli

The role of TNF derived from the experiments was strongly associated with the type of infectious stimuli (Table  4 and Fig.  4 ). The results obtained in the main analyses were also found in the sensitivity analyses, in the subgroups of inactivated TNF experiments, intravenous pathogen injection experiments and intraperitoneal pathogen injection experiments (Supplemental Tables 2, 3, 4).

Animal mortality according to the type of infectious stimulus, with TNF pathway inactivation. Box plot of mortality by experiments, compared using the Mann–Whitney U test. Number of animals: LPS injection: control = 3657, TNF inactivation = 3154; Bacteria: control = 2629, TNF inactivation = 2604; Parasite: control = 232, TNF inactivation = 177; Virus: control = 137, TNF inactivation = 122. LPS: Lipopolysaccharide

LPS injection

LPS injection was the most frequently used model (319 experiments, 42%). LPS was mainly derived from E. coli (75%) and Salmonella species (21%) (Supplemental Table 5). LPS injection was associated with an inappropriate role for TNF in 173 experiments (56%) and with an adaptive role in only 16 experiments (5%). When LPS injection was sensitized by concomitant administration of d -galactosamine, 55 out of 81 experiments (68%) showed an inappropriate role of TNF, and none an adaptive role (Table  4 ).

In the subgroup of experiments with LPS, stimulation of the TNF pathway before LPS injection led to the conclusion of an adaptive role of TNF in 14 out of 24 experiments (58%), whereas inactivation of the TNF pathway led to the conclusion of an inappropriate role in 158 out of 280 experiments (56%) (Supplemental Table 6). This effect was mostly seen when the blocking agent was injected before LPS injection. In experiments involving LPS and TNF pathway inactivation, the relative risk of mortality was 0.66 (95% IC [0.61; 0.72], p  < 0.001) (Supplemental Fig. 1), with significantly higher mortality in the control group than in the inactivated TNF group (94 vs. 33% respectively, p  < 0.001) (Fig.  4 ).

Live bacterial inoculation

Infection models based on live bacterial inoculation were associated with an adaptive role of TNF in 136 out of 306 experiments (44%) and an inappropriate role in only 55 studies (18%). Mortality was higher in the inactivated TNF group than in the control group (75% vs. 50%, p  < 0.001), with a mortality risk ratio of 1.21 (95% CI [1.00; 1.46], p  = 0.005) (Supplemental Fig. 2).

This adaptive role of TNF was particularly observed when Listeria monocytogenes (48/82, 58%) and encapsulated bacteria (61/100, 61%) were inoculated (Table  4 ). A inappropriate role of TNF was observed only in 2 experiments with Listeria monocytogenes , which investigated the role of TNF injection in reducing mortality 48 h after CLP [ 21 ], and was not observed in any experiment with Klebsiella pneumoniae, Salmonella sp, Legionella sp or Streptococcus pneumoniae . Moreover, the difference in mortality was particularly pronounced for these bacteria. When L. monocytogenes , Salmonella species or S. pneumoniae were inoculated, the inactivated TNF group had respectively an increased relative risk ratio of mortality of 4.43 [2.87; 6.83] ( p  < 0.001), 3.76 [1.25; 11.31] ( p  < 0.029) and 1.88 [1.25; 2.84] ( p  < 0.004), respectively (Supplemental Figs. 3, 4, 5, 6, 7).

No role for TNF could be determined in experiments with Pseudomonas aeruginosa , an organism commonly involved in nosocomial infections, except in pneumonia, the most common clinical infection with this pathogen, where an adaptive role of TNF was observed in 55% of experiments (5/9) (Supplemental Table 7).

Importantly, in all these experiments, inoculum analysis showed that high initial bacterial loads were strongly associated with an inappropriate role of TNF, whereas low loads were associated with an adaptive role: 9 × 10 9 colony forming units per kg (CFU/Kg) [4 × 104-4 × 1010], vs. 10 6  CFU/kg [2 × 10 5 –4 × 10 8 ], respectively. Antibiotic therapy, which was mainly used in experiments with high initial inoculum (9 × 10 9  CFU/Kg [2x109-3x1010]), was also associated with an inappropriate role of TNF. In the meta-analysis approach, the risk ratio of mortality when both TNF was inactivated and antibiotic were administrated was 0,69 [ 74 ] ( p  < 0,001) (Supplemental Fig. 8).

Parasite & fungus inoculation

Candida species was the most common pathogen of this group. The other two pathogens used were Histoplasma spp. and Plasmodium berghei. As with live bacteria, in the conclusive experiments, inoculation of parasites and fungi was strongly associated with an adaptive role of TNF (Table  4 ). However, no significant difference in mortality was observed (Fig.  4 and Supplemental Fig. 9).

Virus injection

The main viruses studied were influenza [ 22 , 23 , 24 , 25 ] and dengue [ 26 , 27 , 28 ] using mice with altered interferon pathways. Viral infections were associated with an inappropriate role of TNF in 54% of experiments, with no significant difference ( p  = 0.097) (Table  4 ). While a difference in mortality was initially observed (Fig.  4 ), this difference disappeared when the weighted pooled risk ratio of mortality analysis was performed (Supplemental Fig. 10). A study investigating the role of TNF in cytomegalovirus (CMV) meningoencephalitis [ 29 ] reported 13 experiments showing an adaptive role of TNF when injected before infection and an inappropriate role of TNF when injected after infection.

Multivariate analysis

To more objectively define the main factors associated with the role of TNF, two multivariate analyses were performed: the first to determine the adaptive role of TNF and the second to determine its inappropriate role (Fig.  5 and Supplemental tables 8 and 9). Both analyses yielded comparable results: pneumonia, CLP, and live bacterial inoculation (especially encapsulated bacteria and Listeria monocytogenes), were strongly associated with an adaptive role of TNF, whereas concomitant LPS (especially LPS and galactosamine) and antibiotic injection were strongly associated with an inappropriate role of TNF.

Forest plot of multivariate analysis determining role of TNF. Odds ratios and confidence intervals were calculated using a binary regression model. The interest variable was the adaptive role of TNF ( A ) and the inappropriate effect of TNF ( B ). In model A, the variable ‘adaptive role of TNF’ was coded as 1 for experiments that found an adaptive role of TNF and 0 for experiments that found an inappropriate or a non-significant role. In model B, the variable ‘inappropriate role of TNF’ was coded as 1 for experiments that found an inappropriate role of TNF and 0 for experiments that found an adaptive or a non-significant role. Number of experiments included in both analyses: 760. R2 Tjur model A: 0.310. R2 Tjur model B: 0.293. The details of the Odds ratio are given in Supplemental tables 8 and 9. In model A, LPS (Lipopolysaccharides) referred to a variable that comprised all experiments that used LPS (LPS alone or with adjuvant like galactosamine). List of variables included in both initial models: Female, Mice, Rat, Monkey, Intraperitoneal injection, Cecal ligature and puncture, Pneumonia, LPS, LPS alone, LPS and galactosamine, Alive Bacteria, Encapsulated bacteria, Listeria monocytogenes, Streptococcus pneumonia, Parasite & fungus, Virus, Antibiotherapy, TNF pathway stimulation, TNF pathway inactivation, Anti-TNF antibody, TNF soluble receptor, Blocking TNF before infection, Blocking TNF simultaneous

Contradictory roles of TNF.

Sixteen studies reported a paradoxical role of TNF depending on the experimental model (Table  5 ). Ten studies showed a different role of TNF when LPS injection was compared with infections induced by live bacteria [ 30 , 31 , 32 ], most commonly L. monocytogenes [ 21 , 33 , 34 , 35 , 36 , 37 , 38 ] . As early as 1989, a study showed: an adaptive role of TNF when an encapsulated E. coli (resistant to phagocytosis) was injected, no role when the same microorganism without capsule was injected, and finally an inappropriate role when LPS derived from the same E. coli was injected [ 30 ].

Risk of bias results

Risk of bias assessment revealed biases in all studies (Online Appendix 6 ). Randomization was used in 20 out of the 141 studies (16%) that did no used KO animals. Blinded analysis was conducted in 9 (5%) studies. The number of animals used was unclear in 16 (9%) studies and missing in 31 (18%) studies. Mortality statistics were missing or inadequate in 62 (35%) studies and Fisher’s test was used instead of log-rank test in 42 (24%) studies. Information on the initial bacterial load of the pathogen and its justification was missing in 45 (26%) studies. Additionally, 88 (50%) studies did not simultaneously measure cytokine and bacterial loads, thus only investigating one aspect of infection. Finally, some models are difficult to interpret, such as that of P. aeruginosa enteric infection in neutropenic animals, in which the normal microbiota was profoundly altered after several days of antibiotic therapy. P. aeruginosa, an aerobic microorganism, is rarely associated with digestive infections but is typically found in pneumonia [ 39 ]. For this organism, models of digestive translocations show an inappropriate role of TNF, whereas models of pneumonia show an adaptive role.

The objective of this meta-analysis was to identify the factors that influence the effect of TNF in endotoxemia and sepsis animal models. Its primary finding is the significant association between the effect of TNF and experimental parameters. These parameters include the animal species, their genetic background, the method used for experimental modulation of the TNF pathway, the sequence of injection of modulation agent of the TNF pathway, the type of pathogen, and the infection model used. The variety of these parameters, which may interact in divergent ways, may explain why most experiments (41%) did not provide a clear conclusion regarding the role of TNF.

However, when considering the conclusive experiments, an apparent pattern emerges suggesting that TNF typically exerts an adaptive role unless the immune system is experimentally overwhelmed by a sudden and intense infectious stimulus (e.g., LPS as a superantigen), in which case TNF appears to be detrimental. Consequently, TNF tends to play an inappropriate role in models that induce rapid and high mortality rates, such as infectious models that use remarkably high pathogen loads or direct injections of LPS. These models are rarely representative of the situations encountered in clinical practice, which should serve as the basis for understanding the pathophysiological role of key players. In contrast, TNF appears to play an adaptive role in models that more closely mimic sepsis scenarios encountered in clinical practice, such as pneumonia or CLP. However, these findings must be interpreted with caution due to their important level of bias and their limited relevance to the standards of good practice expected in clinical trials, such as randomization and blinding.

The results of this systematic review are illustrated by the 1987 study by Tracey et al. [ 40 ], which was the first to suggest an inappropriate role for TNF using live bacteria ( E. coli ). In this study, a laboratory strain of E. coli was administered at a dose greater than 1.2 × 10 [ 12 ] bacteria inoculated intravenously over 30 min, in conjunction with early administration of antibiotics. However, this initial inoculum does not appear to be physiological. In fact, feces, the natural element containing the highest concentration of E. coli , typically has concentrations around 10 8 Enterobacterales per gram [ 41 ]. Consequently, the bacterial load used in this study would be equivalent to 10 kg of feces. The authors did not provide any justification for the choice of such a dose, and it is difficult to imagine such a scenario occurring in nature, especially via intravenous administration. In addition, the rapid use of antibiotics makes these models more akin to acute inflammation models, similar to LPS injection, with extremely high TNF levels, exceeding those found in more physiological models such as CLP [ 42 ]. For instance, in the 1985 article by Beutler et al. [ 2 ], which was the first to suggest an inappropriate role of TNF in infections, LPS was progressively injected until lethality was induced. However, the lethal dose was not compared with the circulating levels of LPS found in clinical situations of infection. Other studies have also investigated this subject and found relatively low circulating levels. In their 2003 study, Echtenacher et al. found that 48 h after a CLP, the concentration of LPS in serum was 0.358 ng/ml in mice [ 21 ]. However, after the injection of just 1 µg of LPS, the concentration increased to 1004 ng/ml, which is 3000 times higher. Remarkably, this dose of LPS did not induce any mortality, with the lethal dose being at least 100 µg/ml, i.e., 300,000 times higher than the concentrations observed in physiological CLP situations. This is in line with studies that evaluate circulating LPS levels in humans. In the first study to measure circulating endotoxins in human sepsis [ 43 ], only 17% of patients had endotoxemia, and at relatively low concentrations (5 to 0.5 ng/ml). This result has been confirmed by more recent studies [ 44 , 45 ].

Additionally, 25% of LPS experiments involve the injection of galactosamine along with LPS. Galactosamine is used to sensitize mice to LPS and reduce the amount needed to cause mortality. Unlike other species such as rabbits, mice are highly resistant to LPS and require large doses to be lethal [ 46 , 47 ]. However, galactosamine can induce fulminant hepatitis [ 48 ] by sensitizing hepatocytes to LPS, resulting in significant apoptotic cell death of nearly all hepatocytes [ 49 ]. This mechanism differs from the mortality induced by LPS. Indeed, mice resistant to the association LPS-galactosamine [ 50 ] present the same mortality rate than wild-type mice to LPS injection [ 51 ]. As LPS accounts for 40% of the experiments and is the main infectious stimulus assessing the role of TNF, this could explain why this cytokine is often considered to be inappropriate in sepsis [ 52 , 53 ]. Nowadays these limitations of LPS are known, and LPS is no longer recommended for studying sepsis [ 54 , 55 , 56 ]. However, sepsis definitions are still partially based on these results. Sepsis is defined as a dysregulated host response to infection [ 18 ], whereas experimental data that focused on particularly virulent bacteria found, on the contrary, an adaptive role of TNF.

In our review, experiments with virulent bacteria, which used much lower initial inocula, appear to more closely reflect the situations observed in clinical contexts. For instance, L. monocytogenes , a pathogen that is well-known for inducing meningitis and maternal–fetal infections, was the primary organism used and was strongly associated with an adaptive role of TNF. The initial intravenous dose varied between 10 2 and 10 5  CFU (10 4 –10 7  CFU/Kg). However, the threshold for food contamination with L. monocytogenes is set at 100 CFU/g of food [ 57 ]. The doses used in these articles corresponded to quantities of contaminated food ranging from 1 g to 1 kg, which are more realistic scenarios than the bacterial load used with E.coli as previously mentioned [ 40 ]. The use of encapsulated bacteria was associated with even lower doses of pathogens. Cross et al. [ 30 ] found that less than a dozen encapsulated E. coli bacteria were sufficient to kill all the TNF KO mice, while the control mice died with a bacterial load 10 5 times higher (5 × 10 5  CFU/kg) CFU. In contrast, the same E. coli lacking the capsule required an inoculum of about 10 7  CFU (5 × 10 8  CFU/kg) to induce mortality in all the mice, with no difference observed between the TNF KO and control mice. The capsule appears to cause mortality variations that are equally significant as the absence of TNF. Capsules are commonly present in E. coli bacteria and act as virulence factors that are prevalent in clinical settings, particularly in neonatal meningitis and urinary tract infections [ 58 , 59 ]. Due to their capsule, these bacteria are resistant to phagocytosis and the complement pathway, particularly in children [ 60 , 61 ]. These findings are consistent with experiments demonstrating increased invasiveness of encapsulated E. coli compared to non-encapsulated E. coli [ 59 , 62 ]. Additionally, E. coli encountered in clinical settings can produce toxins such as Shiga toxin, contributing to their high virulence [ 63 , 64 ]. Overall, these results underscore that laboratory bacterial strains are unable to induce the same level of sepsis as the virulent bacteria encountered in clinical settings. A prime example of this is S. pneumoniae , which is the microorganism most commonly found in young and elderly patients. Despite the use of antibiotic therapy and the development of pneumococcal vaccination, pneumococcal infection remains a leading cause of bacterial pneumonia and community-acquired meningitis, and almost 800,000 children under the age of five die each year worldwide from this infection [ 65 ]. In our review, no study found an inappropriate role of TNF in relation to this pathogen. For example, in two studies, a dose of 100 pneumococci injected intraperitoneally was sufficient to kill more than 80% of Tnfr1 - KO mice, whereas 10 7  CFU were required to induce similar mortality in control mice [ 66 , 67 ]. These results support the notion that TNF plays an adaptive role in pneumococcal infections, which is consistent with other experimental studies involving animals lacking genes encoding molecules such as IL-1B [ 68 ], TLR-4 [ 69 ] and TLR-2 [ 70 ], TLR-9 [ 71 ] and MYD88 [ 72 , 73 ].

When interpreting experiments that report lethal injections of TNF, the dose must also be considered. In the 1987 study by Tracey et al., the administered dose of TNF required to induce mortality in 50% of the rats was 0.6 mg/kg, resulting in a peak plasma TNF concentration of 600 ng/ml. In the study by Rothe et al., the dose required to induce mortality in 50% of the mice was 1 µg per mouse, equivalent to 0.05 mg/kg, resulting in an estimated peak plasma TNF concentration of 66 ng/ml [ 33 ]. These levels of circulating TNF are significantly higher than those found in septic patients, which typically do not exceed 0.1 ng/ml [ 4 , 11 , 57 , 58 ]. Furthermore, Feuerstein et al. found that injection of recombinant TNF at concentrations 10–100 times higher (10 7 UI/ml) than those found in rats succumbing to LPS injection did not result in lethality [ 76 ]. Some experimental models based on E. faecalis [ 77 , 78 ], with mortality rates exceeding 50%, have failed to detect measurable levels of TNF. Furthermore, in the 1989 study by Sheppard et al., the injection of 50 µg/ml TNF in rats, resulting in a peak concentration of approximately 50 ng/ml, was not inappropriate but rather adaptive, shielding the animals from a lethal injection of LPS administered 24 h later [ 79 ]. In the same year, Hershman et al . conducted a study wherein the administration of 0.1 µg of recombinant TNF, resulting in an estimated peak concentration of 6 ng/ml, exhibited an adaptive effect by increasing the survival rate of mice with K. pneumoniae skin infection [ 80 ]. These experimental findings suggest that remarkably high levels of TNF, well above those typically observed in septic patients, may not only be compatible with life but may also confer an adaptive effect during infection. This phenomenon may be related to increased secretion of soluble TNF receptors, which may attenuate the increase of TNF, except during the very early stages of infection [ 81 ]. This may help elucidate why certain studies in the mid-1990s showed that circulating TNF levels were not correlated with mortality and could even be adaptive in human sepsis [ 82 , 83 ].

It is important to acknowledge that our meta-analysis is constrained by certain limitations inherent to the nature of the included studies. Primarily, most of the studies were not randomized (84%) or blinded (95%), which introduces the possibility of bias in the analysis. These percentages are consistent with those reported in a 2011 meta-analysis on bias in experimental studies that included 277 experimental studies conducted between 1999 and 2005, which found rates of 87% and 86%, respectively [ 84 ]. However, a more recent meta-analysis focusing on animal studies in cardiology from 2006 to 2016 found better rates (78% and 67%), suggesting some improvement over time [ 85 ]. Furthermore, no study included a calculation for sample size. Therefore, the non-significant effect that was the main effect observed in our meta-analysis may be attributed to the small number of animals included in the experiments. However, the number of animals per experiment was not associated with the type of TNF effect (Table  1 ) thus the lack of statistical significance may be linked to a non-optimized experimental protocol. Of course, the lack of rigorous methodology can result in erroneous conclusions, as illustrated by Perrin and colleagues in their study on amyotrophic lateral sclerosis [ 86 ]. Nonetheless, this is likely to have minimal impact on the overall findings of our study, as there seems to be a general consistency across the studies. None of them indicated that injecting low doses of LPS or virulent microorganisms, such as encapsulated bacteria, was associated with an inappropriate of TNF. On the other hand, ten of the studies included highlighted the dual role of TNF. It was found to be adaptive in the case of infection, but inappropriate when LPS was administered (Table  5 ). The contrasting role of TNF in response to LPS and E. coli injection compared to more virulent pathogens such as S. pneumonia and Listeria spp was also highlighted in a systematic review conducted in 2005 [ 87 ].

A further crucial aspect of this study is the low rate of antibiotic utilization, which was observed in 10% of all experiments and in 20% of experiments involving live bacteria and was associated with an inappropriate effect of TNF in our meta-analysis. In clinical practice, antibiotics are the primary treatment for sepsis in humans. However, it is essential to acknowledge that antibiotics can disrupt the immune response by triggering the release of LPS, leading to elevated levels of TNF and IL-6. Furthermore, the bactericidal properties of antibiotics limit the beneficial effects of TNF release and its adaptive impact, thus emphasizing the visualization of the inappropriate effects.

Finally, our meta-analysis has limitations associated with its conception. Although we aimed to be as inclusive as possible, our literature search strategy may not have been able to include all articles where both the TNF signaling pathway was altered and mortality was assessed. Moreover, almost 6% of the eligible publications could not be analyzed because the articles were not locatable. However, half of these articles were not written in English and might have minimal impact on the current opinion. Nonetheless, this investigation, comprising 175 studies, represents the largest meta-analysis on this topic to date.

Our statistical approach, particularly our multivariate analyses, can also be discussed. Firstly, observations must be independent to be included in the logistic regression, but this assumption may be invalid, as several experiments within each study were included. However, it is currently impossible to evaluate the dependence of observation, and several studies have found different effects of TNF based on the experimental protocol. Therefore, this potential bias may have minimal impact on our multivariate analyses.

Moreover, achieving a completely objective selection of variables for the multivariate analysis is challenging. To address the subjectivity in the variable selection process, we conducted two separate analyses: one focusing on the adaptive effect and another on the inappropriate effect, both yielding comparable results. Furthermore, the predictive values of these multivariate analyses were reasonable (R2 Tjur around 0.3), but this indicates that many experiments are not well classified by our model. The lack of discrimination in our model may be due to the high proportion of non-significant experiments (41%). However, our three statistical approaches consistently point in the same direction. Hence, we believe the risk of error in our main results, as described in the conclusion and visual abstract, is extremely low.

The role of TNF during infection, whether adaptive or inappropriate, varies depending on the experimental model used. Models based on virulent bacteria, which result in high mortality even at low inocula, have demonstrated the adaptive role of TNF. Conversely, models based on LPS or low-pathogenic live bacteria, administered at doses well above physiological thresholds and combined with early antibiotic therapy, have been associated with an inappropriate role of TNF on survival. As the first mentioned models are closest to the conditions encountered in clinical practice, this meta-analysis suggests that TNF may play an adaptive role in infections. This observation may explain the lack of efficacy of anti-TNF treatments in sepsis. Indeed, the rationale behind the administration of such drugs is based on a poor pathophysiological understanding of sepsis, as experimental models with low-pathogenic bacteria do not allow to elucidate the mortality of virulent bacteria.

Data availability

Files with data extraction and R statistical analysis code are available on request.

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Long-Term Effects of Childhood Exposure to War on Domestic Violence

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• Joseph B. Ajefu 1 , 2 &
• Daniela Casale 3  

This paper highlights the scarring effects of early life exposure to civil war, by examining the impact of exposure to conflict in childhood on the incidence of domestic violence in adulthood among married women. To estimate these effects, we use a difference-in-differences model which exploits variation in exposure to Nigeria’s 30-month-long civil war by year of birth and ethnicity. Our results, based on the 2008 Nigerian Demographic Health Survey, show that women exposed to the war during childhood are more likely to be victims of domestic violence in adulthood compared to those not exposed to the war, with larger effects observed for those exposed at younger ages. Additionally, we explore the mechanisms through which exposure to civil war might affect domestic violence and find some support for both the normalisation of violence and weakened bargaining power hypotheses. Understanding the root causes of domestic violence is important given the high prevalence in developing countries and the deleterious consequences for women and their children.

Ce document met en évidence les effets cicatrisants d'une exposition précoce à la guerre civile, en examinant l'impact de l'exposition au conflit pendant l'enfance sur l'incidence de la violence domestique à l'âge adulte chez les femmes mariées. Pour estimer ces effets, nous utilisons un modèle de différences en différences qui exploite la variation de l'exposition à la guerre civile nigériane de 30 mois en fonction de l'année de naissance et de l'ethnicité. Nos résultats, basés sur l'Enquête démographique de santé nigériane de 2008, montrent que les femmes exposées à la guerre pendant l'enfance sont plus susceptibles d'être victimes de violence domestique à l'âge adulte par rapport à celles qui n'ont pas été exposées à la guerre, avec des effets plus importants observés pour celles exposées à des âges plus jeunes. De plus, nous explorons les mécanismes par lesquels l'exposition à la guerre civile pourrait affecter la violence domestique et trouvons un certain soutien pour les hypothèses de normalisation de la violence et d'affaiblissement du pouvoir de négociation. Comprendre les causes profondes de la violence domestique est important étant donné la prévalence élevée dans les pays en développement et les conséquences délétères pour les femmes et leurs enfants.

Este documento destaca los efectos perjudiciales de la exposición en los primeros años de vida a la guerra civil, examinando el impacto de la exposición al conflicto en la infancia sobre la incidencia de la violencia doméstica en la adultez entre mujeres casadas. Para estimar estos efectos, utilizamos un modelo de diferencias en diferencias que explota la variación en la exposición a la guerra civil de Nigeria de 30 meses de duración por año de nacimiento y etnia. Nuestros resultados, basados en la Encuesta de Salud Demográfica de Nigeria 2008, muestran que las mujeres expuestas a la guerra durante la infancia tienen más probabilidades de ser víctimas de violencia doméstica en la adultez en comparación con aquellas que no estuvieron expuestas a la guerra, con efectos mayores observados para aquellas expuestas a edades más tempranas. Además, exploramos los mecanismos a través de los cuales la exposición a la guerra civil podría afectar la violencia doméstica y encontramos cierto apoyo tanto para las hipótesis de normalización de la violencia como para el debilitamiento del poder de negociación. Comprender las causas fundamentales de la violencia doméstica es importante dado su alta prevalencia en los países en desarrollo y las consecuencias perjudiciales para las mujeres y sus hijos.

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Introduction

Since World War II, almost one-third of all countries have experienced civil war, and the incidence of armed conflict has been on the rise (Gleditsch et al. 2002 ). In Sub-Saharan Africa specifically, nearly three-fourths of countries in the region have experienced civil war (Gleditsch et al. 2002 ). These conflicts have often led to considerable loss of lives, deterioration of physical and human capital, erosion of institutional capacity, and reduced economic growth (Akbulut-Yuksel and Yuksel 2017 ). It has been estimated, for instance, that between 2012 and 2017, the global economic costs of conflict increased from $12.62 trillion to $14.76 trillion, with many of the conflict-torn countries trapped in a perpetual cycle of violence (World Development Report 2011 ; World Humanitarian Data and Trends Report 2017 ; Institute for Economics and Peace 2018 ).

While the macroeconomic costs of war have long been studied in economics, literature on the microeconomic impacts of civil war, particularly in developing countries, has grown in the last 20 years especially, perhaps as more data have become available (Verwimp et al 2019 ). Studies have shown that exposure to conflict is negatively associated with educational attainment (Singh and Shemyakina 2016 ; Chamarbagwala and Moran 2011 ; Shemyakina 2011 ; Swee 2015 ), health outcomes (Akresh et al. 2012a , 2012b ; Grimard and Laszlo 2014 ; Weldeegzie; 2017 ), social trust (Kijewski and Freitag 2018 ), and labour market outcomes (Galdo 2013 ; Islam et al. 2016 ).

In this paper, we add to this literature by exploring how exposure to conflict in childhood affects experiences of domestic violence among women in adulthood, using the case of the Nigerian civil war. Recent work suggests that exposure to war increases women’s likelihood of experiencing intimate partner violence across a range of contexts. La Mattina ( 2017 ) finds that exposure to the genocide in Rwanda increased the incidence of domestic violence among women who married after 1994 compared to those who married before the genocide occurred, with a larger effect for women in areas with high genocide intensity. Kelly et al ( 2018 ) match district-level information on conflict-related fatalities during the civil war in Liberia from 1999 to 2003 to data on post-conflict intimate partner violence from the 2007 Demographic Health Survey (DHS). They find a strong effect of fatalities on the incidence of intimate partner violence, with 4–5 years of cumulative exposure having the strongest effect. In a similar vein, Østby et al ( 2019 ) analyse the experiences of women in Peru during and after the civil war from 1980 to 2000 and find that those living in areas with higher exposure to conflict-related violence are at increased risk of violence in the home. Svallfors ( 2023 ) analyses DHS data from 2005 to 2015 for Columbia and shows that local-level exposure to armed conflict events in the previous year especially, increased women’s likelihood of experiencing intimate partner violence.

In all these studies, the focus has been on the association between conflict exposure and domestic violence in adulthood, or on temporally proximate relationships. In our reading of the literature, we could find only one very recent published paper by Torrisi ( 2023 ) which tries to uncover whether the timing of exposure matters, and particularly whether exposure to armed conflict during childhood has long-lasting consequences for domestic violence in adulthood. Torrisi ( 2023 ) combines DHS data with geo-referenced information on the armed conflicts that occurred in four ex-Soviet countries (Armenia, Azerbaijan, Moldova, and Tajikistan) soon after the break-up of the USSR. She finds that women who were exposed to conflict by age 19 were more likely to experience domestic violence than those never exposed or not exposed by age 19, and that this effect is driven largely by exposure in the sensitive childhood period from 0 to 10 years of age (with no significant effect for those exposed at ages 11 to 15 or 16 to 19).

We also found two working papers that explore the relationship between childhood exposure and domestic violence in adulthood (Gutierrez and Gallegos 2016 ; La Mattina and Shemyakina 2017 ). Gutierrez and Gallegos ( 2016 ) use DHS data from Peru coupled with information on geographical variation in exposure to violent conflict to show that both women who were exposed at ages 0 to 8 and 9 to 16 experienced a higher incidence of domestic violence in adulthood compared to those not exposed. La Mattina and Shemyakina ( 2017 ) use the DHS data on selected Sub-Saharan African countries and exploit both temporal and geographical variation in conflict intensity between 1946 and 2006 across sub-national regions. Their results suggest that women who live in a region where there was an armed conflict when they were 6 to 10 years old are more likely to experience domestic violence than individuals not exposed to conflict by age 20, but they do not observe similar effects for individuals who were exposed to conflict at ages 0 to 5 or 11 to 20.

There is a common methodological thread that runs throughout all these studies: they use geo-referenced data on conflict-related violence combined with post-conflict data on domestic violence from the DHS surveys. In addition to imperfect matching at the sub-national or district level due to differences in levels of geographical disaggregation or demarcation between the two sources of data, a key concern with this approach is endogenous migration. The DHS only has information on the individual’s current place of residence and not on their residence in childhood or at the time of conflict. There is therefore no guarantee that the women who are currently living in a previously conflict-exposed area were also living there during childhood when the conflict took place. Indeed, endogenous migration is likely to be more of a concern during times of conflict, and the direction of the effect is difficult to predict. It is possible that the most vulnerable women (and men) may be displaced or forced to flee with their families during times of conflict, but it is also possible that the least vulnerable, those with better economic resources and social networks, are the ones who can more easily relocate to places of safety. To try and address this problem, many of the studies listed above restrict their samples to those who had never moved since birth or who had not moved in the previous five years, depending on the data available in the DHS. In doing so, however, they tend to lose 50 percent or more of their initial sample (Gutierrez and Gallegos 2016 ; La Mattina and Shemyakina 2017 ; Torrisi 2023 ), likely leading to biassed results.

Our paper makes a useful methodological contribution to this growing literature on the long-term effects of war exposure by using what we consider to be a more robust method of identifying exposure than the commonly used geographical approach. We use ethnicity and birth cohort to identify exposure to conflict in childhood during the Nigerian civil war (following the approach adopted in Akresh et al 2012a , 2023 ). We are able to adopt this approach because of the very specific nature of the Nigerian civil war, which occurred from 6 July 1967 to 15 January 1970, and which was restricted to the south-eastern region of Nigeria inhabited by the Igbos and other minority ethnic groups (which we will describe in more detail below). This strategy mitigates the problem of selective migration associated with the use of geography-based variables to identify exposure, a problem which is likely to be more pronounced during times of conflict.

In addition, we examine exposure in early childhood using more granular age ranges than have currently been explored, namely those exposed in utero, between the ages of 0 to 4, 5 to 8, and 9 to 12. In doing so, we add to the growing body of literature in economics which recognises that there are long-run implications of early life shocks and that adverse circumstances during the sensitive early period of childhood can impact a range of later life outcomes (Case et al. 2005 ; Cunha and Heckman 2007 ; Almond and Currie 2011 ; Currie 2020 ). This includes increasing evidence that in utero exposure to shocks such as war, disease, and famine have long-term negative consequences on physical and mental health, educational attainment, earnings, and other socio-economic outcomes (Almond 2006 ; Camacho 2009 ; Almond and Currie 2011 ; Comfort 2016 ; Almond et al. 2018 ).

Finally, we try to unpack the mechanisms through which early life exposure to conflict affects experiences of domestic violence in adulthood, using the rich data available in the Nigerian Demographic Health Survey. We explore two possible channels. The first, the normalisation of violence hypothesis, relies on the well-known finding that children who witness violence at home are more likely to become a victim or perpetrator of domestic violence themselves in adulthood (Schwab-Stone et al. 1995 ; Gage 2005 ; Yount and Li 2009 ; Cesur and Sabia 2016 ; Jin et al. 2017 ). If war results in more intimate partner violence among married couples, as the evidence presented earlier suggests, we would expect children growing up during war to witness more violence among their parents than observably similar children. Even if children do not witness violence within their own homes, one might expect that children exposed to community-level violence through war during their formative years might also be more likely to view violence as a justifiable response to certain problems (Barnett et al. 2005 ; Fowler et al. 2009 ; Gutierrez and Galegos 2016 ). To examine whether exposure to violence in childhood might have affected the formation of beliefs during the critical early years, we use data in the DHS on whether war-exposed women witnessed domestic violence in their homes as children and on women’s and men’s attitudes towards wife-beating in adulthood (Huber 2023 ).

The second hypothesis we explore is reduced bargaining power in the household, which would affect women’s options outside of the marriage and in turn increase their likelihood of being victims of domestic violence (Bhattacharyya et al. 2011 ; Heath 2014 ; La Mattina 2017 ). There are a number of reasons why women exposed to war may have fewer outside options. For instance, a number of studies in a range of countries have found evidence that civil conflict results in poorer educational outcomes (Akresh and Walque 2008 ; Leon 2012 ; Shemyakina 2011 ; Chamarbagwala and Moran 2011 ; and Dabalen and Paul 2014 ), and there is some evidence that exposure to conflict negatively affects girls more than boys (Singh and Shemyakina 2016 ). Women with lower education have fewer out-of-marriage options given their weaker labour market outcomes and increased financial dependence on their husbands, raising the likelihood of domestic violence (Lundberg and Pollak 1996 ; Farmer and Tiefenthaler 1997 ; Aizer 2010 ; Bhattacharyya et al. 2011 ; Eswaran and Malhotra 2011 ; Galdo 2013 ; Heath 2014 ). Moreover, war exposure can affect marriage, reproductive and health outcomes, which would have consequences for women’s intra-household bargaining power (Verwimp and van Bavel 2005 ; Aizer 2011 ; Akresh 2012a ; Islam et al 2016 ; Cetorelli and Khawaja 2017 ; La Mattina 2017 ). To measure women’s bargaining power in adulthood, we use the information in the DHS on women’s decision-making power in the household across a number of domains (Ajefu and Casale 2021 ).

Our main findings are as follows. We find that women exposed to the Nigerian civil war during childhood are more likely to be victims of domestic violence in adulthood compared to women not exposed to the civil war. Specifically, we find that exposure to the civil war is associated with an increase in the likelihood of being a victim of domestic violence of 1.2 percentage points compared to non-exposed cohorts (or 6% given the sample mean incidence of 19.7%). These effects appear to be more pronounced the earlier on one is exposed in childhood, with particularly large effects for those exposed in utero. While it is far more difficult to identify the channels through which exposure to the civil war affects domestic violence (particularly across the cohorts), in our exploratory work, we find some evidence to support both the normalisation of violence and bargaining power hypotheses.

The rest of the paper is structured as follows. Section 2 provides background information on the Nigerian civil war. Section 3 discusses the data and the empirical identification strategy, and presents some descriptive statistics. Section 4 presents the estimation results, and Sect. 5 concludes.

Background on the Nigerian Civil War

Under British colonial rule, Nigeria comprised three regions, namely the northern, western, and eastern regions. Footnote 1 Each of these regions had a predominant ethnic group, with the Hausa in the North, the Yoruba in the West, and the Igbo in the East. Like many countries in Africa, political and social conflict in Nigeria bore both ethnic and regional dimensions (Simpson 2014 ). In less than seven years after becoming an independent nation (on 1 October 1960), some of these long-standing tensions between the different groups intensified and the country was plunged into a civil war, also known as the Biafran War.

While the underlying geo-political causes of the war are too complex to explain here, some of the immediate causes of the Nigerian Civil War were the military coup on 15 January 1966, organised by primarily Igbo army officers, the counter-coup of 28 July 1966, and the subsequent persecution and killing of the Igbos in the Northern part of the country (Kirk-Greene 1971 ; Nafziger 1972 ). In response to this, there was a massive return migration of Igbos seeking refuge (estimated to involve around 1.5 million people) to their homeland in the south-eastern region (Aall 1970 ; Akresh et al 2012a ). On 30 May 1967, the south-eastern region declared itself the Republic of Biafra and this led to a full-blown civil war that began on 6 July 1967 (see Fig.  1 ).

Map of Nigeria indicating the south-east states. The civil war was restricted to the south-east region that declared itself the Biafra republic

Nigeria’s Federal Military Government fiercely resisted the breakaway republic for two and a half years, using both their military might and their ability to impose a blockade of the landlocked territory (preventing the inflow of food, medicine, and other essential supplies). It has been estimated that between 1 and 3 million people died from the violence and mass starvation that ensued, in what was considered one of the bloodiest wars in sub-Saharan Africa (Akresh et al. 2012a ; Simpson 2014 ). The war ended on 15 January 1970 after the Republic of Biafra surrendered to the Nigerian troops.

Two key features of this devastating conflict are salient to our empirical strategy. First, because of the military blockade (which prevented movement of both people and supplies), the war was fought in the south-eastern region with direct civilian exposure largely restricted to this area (Akresh et al. 2012a ). Second, at the time of the war, most Igbos were living in their native states in the south-east, and many of those living outside the area returned there before the war to seek refuge in the mass migration that occurred just before secession was declared (Aall 1970 ). We can therefore use ethnicity and birth cohort to identify exposure to the civil war. This identification strategy is similar to that used by Akresh et al ( 2012a ) in their study on the impact of exposure to the Nigerian civil war on women’s stature in adulthood. This strategy is preferred to using current geographical demarcation, as is the case in other studies exploring the relationship between war exposure and domestic violence, as it circumvents the problem of selective migration (ethnicity is invariant to migration).

To investigate the impact of the Nigerian civil war on women’s experience of domestic violence in adulthood, we use the 2008 Nigerian Demographic Health Survey (DHS). The DHS is a large nationally representative cross-sectional survey conducted in a number of developing countries. It provides information on women between the ages of 15 and 49 years on a large number of demographic and socio-economic factors. The 2008 Nigerian DHS covered 34,070 households and 33,385 women. Footnote 2 We use the 2008 survey in this study for two main reasons: it is the first wave of the Nigerian DHS to collect information on the incidence of domestic violence among women; and given the timing of the war, this particular survey covers the largest sample of war-exposed women, allowing us to explore the effects of exposure in utero through to exposure at 12 years of age. Footnote 3

The information on domestic violence was collected through a specially designed questionnaire that was administered to one randomly selected woman in each household. Footnote 4 Women who were (or had been) married or cohabiting were asked in private about incidents of domestic violence as follows: “(Does/did) your (last) husband ever do any of the following things to you: (a) slap you? (b) twist your arm or pull your hair? (c) push you, shake you, or throw something at you? (d) punch you with his fist or with something that could hurt you? (e) kick you, drag you or beat you up? (f) try to choke you or burn you on purpose? (g) threaten or attack you with a knife, gun, or any other weapon? (h) physically force you to have sexual intercourse with him even when you did not want to? (i) force you to perform any sexual acts you did not want to?” We measure domestic violence using a binary variable that takes the value of 1 if a woman suffered any of the above-mentioned aggressive behaviours from her husband or partner and 0 otherwise.

Empirical Identification Strategy

To estimate the causal impact of exposure to the civil war in childhood on experiences of domestic violence in adulthood, we adopt a difference-in-differences strategy. As described above, our identification strategy exploits variation in exposure to the civil war by birth cohort and ethnicity. This estimation strategy minimises the problem of selective migration associated with the use of geographical variation in conflict exposure and helps to circumvent one of the limitations of the Nigerian DHS, namely, that it only has information on the current residence of respondents but no information on their place of birth or their place of residence during the war.

We define the treatment or war-exposed group as those Igbo and other minority ethnic groups (who would have been in the south-eastern region when the war was fought) born between 1958 and October 1970. These women were between 0 and 12 years old (including in utero) when the war took place between July 1967 and January 1970, and are aged 38 to 49 years in 2008 when we observe their experiences of domestic violence.

We present two distinct control groups: i) one across time, i.e. women from the war-exposed ethnicities but born in the six-year period following the war, namely from November 1970 to December 1976 (and aged 32 to 38 years in 2008), Footnote 5 and ii) one across ethnicity, i.e. the same birth cohorts (1958–1976) but from the non-war-exposed ethnicities (predominant in the other regions of Nigeria). Table 1 summarises birth cohorts for the war-exposed and non-exposed groups, respectively.

We estimate Eq. ( 1 ) below:

where \({\text{Y}}_{\text{ijt}}\) is equal to one (zero otherwise) if individual i belonging to ethnicity j and born in year t was a victim of domestic violence in adulthood. \(wa{r}_{ethnicity}\) denotes Igbo or other minority ethnic groups in the south-east region and \({Cohort}_{it}\) includes four cohorts, namely those exposed to war in utero (born between February and October 1970), those exposed between 0 and 4 years (born 1966–1970), those exposed between 5 and 8 years (born 1962–1965), and those exposed between 9 and 12 years (born 1958–1961), where the omitted category is those born between November 1970 (i.e. nine months after the war) and December 1976. The interactions of war ethnicity with each of the four cohorts are the variables of interest and capture the effect of an individual’s exposure to the civil war on the incidence of domestic violence. \({X}_{ij}\) is a vector of individual and household characteristics, which includes age at first marriage, religion, education, urban residence, and household wealth; \({\delta }_{r}\) is a state fixed effect; and \({\varepsilon }_{ijt}\) is a random, idiosyncratic error term. We estimate the regressions using ordinary least squares (OLS) (although the results are robust to using probit regressions), and standard errors are clustered at the ethnicity level to account for serial correlation (Bertrand et al. 2004 ).

Summary Statistics

Table 2 reports the summary statistics for our sample of married/cohabiting women from whom domestic violence data were collected. The average age of women in this sample was 39 years, the average age at first marriage was 19 years, around 47% of women in the sample had completed at least primary education, and 32% were resident in urban areas. Among the women who were surveyed, 20% said they had experienced at least one type of domestic violence from their partner.

To explore the normalisation of violence and bargaining power hypotheses as potential mechanisms through which exposure to conflict affects the incidence of domestic violence, we also examine data on attitudes towards domestic violence, domestic violence among parents, and decision-making in the household. The summary statistics for these variables are also shown in Table  2 . On average, 34% of the women in the sample responded that domestic violence is justified if the woman goes out without informing the husband/partner, 32% felt it was justified if a woman neglects the children, 29% felt it was justified if a woman argues with her husband/partner, 26% felt it was justified if a woman refuses to have sex with her husband/partner, and 17% justified violence if a woman burns the food. Nearly 13% percent of women reported witnessing domestic violence among their own parents. In terms of household decision-making, 12% of women reported having the final say on own health care, 7% reported having the final say on large household purchases, 20% reported having the final say on household purchases for daily needs, and 14% reported having the final say on visits to family or relatives.

Table 3 shows that are large and significant differences in these variables by war exposure. Just under 18% of the non-exposed group reported being victims of domestic violence, compared to 27% of the war-exposed group. Moreover, 11% of the non-exposed group witnessed domestic violence among their parents, compared to 19% of the war-exposed group. There are also statistically significant differences in attitudes towards domestic violence, with war-exposed women more likely to report that wife-beating was justified in certain circumstances. For example, 15% of the non-exposed group justified wife-beating if a woman refuses to have sex with her partner compared to 30% of the war-exposed group. In terms of household decision-making, statistically significant differences are observed in three out of the four domains, with war-exposed women less likely to report having the final say on own health care, purchases for daily needs and visits to family and friends.

Figure  2 presents a box plot of our main variable of interest, the incidence of domestic violence, across the cohorts. Within each birth cohort, the incidence of domestic violence is clearly higher for the war-exposed ethnic groups compared to the non-exposed ethnic groups, and the difference between the two appears larger for those exposed at younger ages. However, these are unconditional estimates, and it remains to be seen whether these effects will hold in the multivariate difference-in-differences analysis, which we present in the next section.

Box plot showing the incidence of domestic violence across the cohorts for the exposed and non-exposed ethnicities

Exposure to Civil War and Domestic Violence

Table 4 presents the results from a series of equations which estimate the effect of exposure to the civil war in childhood (in utero to age 12) on the incidence of domestic violence in adulthood, without disaggregating by birth cohort. The coefficients on the interaction term suggest a positive and significant effect of war exposure in childhood on the incidence of domestic violence among women in adulthood. The size of the coefficient tends to fall as an increasing number of controls are added between columns 1 and 4. The regression in column 4 includes controls for individual and household characteristics and fixed effects for state, ethnicity, and cohort, and is our preferred specification. The coefficient from this regression suggests that exposure to the civil war increases the likelihood of being a victim of domestic violence by 1.2 percentage points (or 6% given the sample mean incidence of 19.7%). Footnote 6

In Table  5 , we disaggregate exposure to the civil war by birth cohort to test whether the effects of civil war exposure on domestic violence vary by the age at which the women were exposed to the war in childhood. The categories represent those exposed in utero (born between February 1970 and October 1970), those exposed between the ages of 0–4 (born 1966–1970), those exposed between the ages of 5–8 (born 1962–1965), and those exposed between the ages of 9–12 (born 1958–1961). From the estimates, we find that the effects are largest for those exposed at younger ages. Specifically, exposure to the civil war in utero increases the probability of experiencing domestic violence in adulthood by 7.4 percentage points, and exposure to the civil war between 0 and 4 years increases the probability of experiencing domestic violence by 1.7 percentage points (specification 4).

These results are consistent with the increasing evidence described earlier that there are long-run implications of early life shocks and that adverse circumstances during the sensitive early period of childhood impact later life outcomes (Case et al. 2005 ; Cunha and Heckman 2007 ; Currie 2020 ). This includes a growing body of literature showing that in utero exposure to shocks such as war, drought, and famine have long-term negative consequences.

This literature draws on the ‘fetal origins’ hypothesis, which proposes that conditions in utero, particularly nutrition, ‘program’ the foetus with particular metabolic features that can result in disease later on in life (Barker; 1990 , 1995 ). Studies have found evidence to link events or circumstances in utero to birth weight, adult height, disability, heart disease, and obesity, suggesting latent and long-lasting consequences on health outcomes (Ravelli et al 1976 ; Dunn 2007 ; Camacho 2009 ; Almond and Currie 2011 ; Comfort 2016 ). In addition, there is evidence to suggest negative effects on mental health and cognitive function as well as on education, employment, and adult earnings, implying potential neurological involvement (Hoek et al 1998 ; Almond 2006 ; Almond et al. 2018 ).

Almond et al ( 2018 ) summarise a number of ‘biological’ or direct mechanisms through which foetal-origin effects can be generated, including nutritional insults, infectious disease, maternal stress, and alcohol and tobacco use, all of which would likely be more prevalent during times of war. In addition to the direct biological mechanisms, there may be social and economic factors at play that reinforce the negative outcomes. However, as Almond and Currie ( 2011 ) and Almond et al ( 2018 ) point out in their extensive reviews of this wide-ranging literature, more work is needed to disentangle the biological from the more indirect socio-economic mechanisms. Some of examples of these during war could include lack of access to health and policing services, disruption of markets and other key institutions, disturbance of family life, established norms and social networks, and changes to parenting behaviour. We reflect on some of these issues further below when looking at the mechanisms through which exposure to war might affect domestic violence in adulthood.

Robustness Checks

To test the robustness of our difference-in-differences strategy which assumes parallel trends, we estimate two placebo regressions (using similar methods to for e.g. Akresh et al. 2012a ; Gutierrez and Gallegos 2016 and Weldeegzie 2017 ). In the first test (column 1 of Table  6 ), we exclude the main war-exposed ethnicities (Igbo and other ethnic minorities) and placebo-treat the ethnic groups in the northern part of the country (Kanuri, Hausa, and Fulani), with the remaining ethnicities used as the control group. We choose the northern part of the country given the geographical distance from the area where the war was fought. In the second test (column 2), we placebo-treat the cohort born immediately after the civil war (from 1971 to 1976), with the cohort born from 1977 to 1980 used as the control group. Footnote 7 We would not expect an effect for women born after the civil war. Neither of the coefficients on the placebo-treated interaction term in Table  6 is statistically significant, providing support in favour of our identification strategy. Footnote 8

Although we chose to use the DHS 2008 for this study, as it provides the largest sample of women exposed to the war in childhood (from in utero to age 12), we also check whether our main results hold using the later round of the DHS from 2013. Column 1 of Table  7 shows the estimated effect of war exposure in childhood (without disaggregating across the cohorts) when only the 2013 sample is used, and column 2 of Table  7 shows the estimated effect when the 2008 and 2013 samples are pooled. The results remain robust, with the effect even larger at 5.4 percentage points in column 1 and 4.7 percentage points in column 2 (compared to the 1.2 percentage points estimated in column 4, Table  4 , using the same specification).

In column 3 of Table  7 , we disaggregate the war-exposed women into the four birth cohorts using the pooled sample from 2008 and 2013. Footnote 9 Again, we find the strongest effect from exposure in utero of 5.1 percentage points (compared to 7.4 percentage points in column 4 of Table  5 , using the same specification). However, in the pooled sample, we also find a significant effect of exposure by those exposed between 8 and 12 years. On the whole, though, our robustness checks support our main findings, namely that war exposure in childhood results in a higher incidence of domestic violence among women in adulthood, and that exposure in utero appears to have the strongest effect.

Potential Mechanisms Through Which Civil War Affects Domestic Violence

Normalisation of violence.

This section explores two potential mechanisms through which exposure to civil war during childhood may affect the incidence of domestic violence in adulthood. The first is the normalisation of violence hypothesis, which has also been referred to as the intergenerational transmission of violence hypothesis or the model of social learning. Exposure to violence at home during a child’s formative years is known to result in a greater likelihood of being a victim or perpetrator of domestic violence in adulthood (Schwab-Stone et al. 1995 ; Gage 2005 ; Mihalic and Elliott 2007; Yount and Li 2009 ; Cesur and Sabia 2016 ; Jin et al. 2017 ). Along the same lines, one might expect that children exposed to community-level violence during war might also be more likely to view violence as a justifiable response to certain problems (Barnett et al. 2005 ; Fowler et al. 2009 ). In Table  8 , we estimate the effect of women’s exposure to the civil war on the justification of domestic violence to test whether women who were exposed to the conflict in childhood have different attitudes towards domestic violence in adulthood.

Most of the coefficients are positive, many are statistically significant, and some are quite large. In general, the results suggest that, across the birth cohorts, women exposed to the war in childhood are more likely to justify the use of wife-beating than non-exposed women, particularly if the woman argues with her husband, refuses to have sex with him, or burns the food. For example (from row 1), women exposed to war in utero were 2.4 percentage points more likely to justify wife-beating if the woman argues with her husband and 6 percentage points more likely to justify wife-beating if she burns the food, compared to the non-exposed group. The effects are similarly large (and in some cases larger) among those exposed between the ages of 0–4, 5–8, and 9–12, depending on the question asked.

In Table  9 , we use the matched couple’s recode data from the DHS Footnote 10 to investigate the effect of husbands’ exposure to the civil war on the justification of domestic violence in adulthood. This recognises that domestic violence involves both a perpetrator and a victim. Given the high degree of assortative mating by ethnicity in Nigeria, the majority of women who were exposed to the civil war are married to men who were also exposed to the civil war. Indeed, the DHS data indicate that 93.4% of war-exposed women were married to war-exposed men (with only 6.3% of non-exposed women married to war-exposed men). Footnote 11 Because the DHS interviews men aged 15–59, we can disaggregate exposure into in utero, between the ages of 0–4 (born 1966–1970), between the ages of 5–8 (born 1962–1965), between the ages of 9–12 (born 1958–1961), and between the ages of 13–22 (born 1948–1957). The results suggest that compared to non-exposed men, war-exposed men are more likely to justify the use of wife-beating. Although the pattern is not entirely consistent across the five columns, the effect is largest for cohorts of men exposed in utero and between the ages of 9–12 and 13–22.

In addition to being exposed to more community-level violence growing up during war, and marrying men similarly exposed as children, the women exposed to war in childhood may also have been witness to more domestic violence in their own childhood homes or more violent forms of parenting. This could be the case if the stresses and violence of war and the disruption to social norms and family life in turn led to more violence among the parents. The literature summarised in the introduction certainly suggests that intimate partner violence rises during times of war and conflict among married or partnered couples (La Mattina 2017 ; Kelly et al. 2018 ; Østby et al 2019 ; Svallfors 2023 ). The questionnaire asks women if they were aware of domestic violence among their parents, specifically whether the father ever ‘beat’ the mother. We find that 11 percent of women not exposed to the war in childhood were aware of domestic violence among their parents, compared to 19 percent of war-exposed women. This is a substantial and significant difference.

We include this variable as an explanatory variable in the regression and we also interact this variable with the war exposure variables to test whether the effect is stronger for those growing up in the midst of the war. Indeed, in Table  10 , we find a strong positive effect of witnessing domestic violence among one’s parents on the likelihood of becoming a victim oneself in adulthood, and particularly for those exposed to the war in utero. This is a striking result and could suggest that the levels of violence in those war-exposed families where the mother was pregnant were particularly severe, as the combined stresses of war and having another child on the way took their toll. It is also possible that the final months of the war (when these exposed women would have been in utero) were particularly intense, and so the effect on family life more substantial. Finally, disruptions during war to the resources that would ordinarily help mitigate the negative effects of intimate partner violence, such as health and policing services and established social networks, might have exacerbated the experiences of pregnant mothers in particular.

Bargaining Power Hypothesis

The second mechanism we explore is the intra-household bargaining power hypothesis. Women with limited resources tend to have fewer outside options which can result in an increased likelihood that they will be victims of domestic violence (Gelles 1976 ; Aizer 2010 ). The literature on the effects of conflict provides a number of reasons why women exposed to war may have fewer outside options. Civil conflict results in poorer educational outcomes (Akresh and Walque 2008 ; Leon 2012 ; Shemyakina 2011 ; Chamarbagwala and Moran 2011 ; and Dabalen and Paul 2014 ), and there is evidence that exposure to conflict negatively affects girls more than boys in terms of educational outcomes (Singh and Shemyakina 2016 ). Women with lower education have fewer out-of-marriage options given their weaker labour market outcomes and increased financial dependence on their husbands (Lundberg and Pollak 1996 ; Farmer and Tiefenthaler 1997 ; Aizer 2010 ; Bhattacharyya et al. 2011 ; Eswaran and Malhotra 2011 ; Galdo 2013 ; Heath 2014 ). Furthermore, war exposure can affect marriage, reproductive and health outcomes, which would have consequences for women’s intra-household bargaining power and experiences of domestic violence (Verwimp and van Bavel 2005 ; Akresh 2012a; Grimard and Laszlo 2014 ; Islam et al 2016 ; Cetorelli and Khawaja 2017 ; La Mattina 2017 ).

We test whether war-exposed women have lower bargaining power compared to non-exposed women using the information on decision-making in the household as a proxy. Specifically, we examine whether war-exposed women are less likely to have the final say on certain key decisions in the household compared to non-exposed women. The results in Table  11 show that while most of the coefficients are negative, as predicted, not all are significant. The strongest results are for those exposed in utero; exposure to the civil war decreases the probability of these women having a final say on their own health care by 5.4 percentage points, and on household purchases of daily needs by 8 percentage points. There are also some significant effects, ranging between 3.6 and 5.6 percentage points, for those exposed to the war between the ages of 5–8 and 9–12 for a number of the outcomes.

Conclusions and Policy Implications

In this paper, we examine the impact of exposure to war during childhood on women’s experience of domestic violence in adulthood. Unlike other studies that use current geography-based variables to identify exposure to conflict, we are able to use ethnicity and birth cohort given the nature of the Nigerian civil war, thereby mitigating concerns of selective migration. Our results indicate that exposure to the Nigerian civil war during childhood increases the likelihood of women being victims of domestic violence in adulthood, with larger effects for those exposed at younger ages, and particularly large effects for those exposed in utero. This is consistent with evidence to suggest that the early childhood period, including the time in utero, is particularly important for later life outcomes and that shocks during this period can have long-lasting effects.

Understanding the mechanisms through which civil war affects domestic violence is equally as important as identifying the effect itself, especially if effective post-war policies are to be designed to mitigate the deleterious consequences of conflict in developing countries. However, identifying the mechanisms is a much more difficult task with the data available, and therefore, our results can only be interpreted as suggestive.

First, we find that both the women in our sample and their husbands who were exposed to the war during childhood are more likely to perceive domestic violence to be an acceptable behaviour in adulthood than those not exposed to the war. This is in line with the normalisation of violence hypothesis that predicts that those exposed to violence in childhood are more likely to become either perpetrators or victims of domestic violence in adulthood. In addition, we find war-exposed women were more likely to witness domestic violence in their own childhood homes than non-exposed women, and that witnessing domestic violence among their parents is positively correlated with experiencing domestic violence themselves in adulthood particularly among those exposed in utero. It is possible that the combined stresses of war and having another child on the way led to more violent behaviour in the home, or that the final months of war (when these exposed women would have been in utero) were particularly intense, and so the effect on family life more marked. Footnote 12

Second, our findings suggest that women who were exposed to the war in childhood also have lower intra-household bargaining power compared to non-exposed women, which would make them more vulnerable to incidents of domestic violence. Relative to the non-exposed group, we found women who were exposed to the conflict in childhood have less decision-making power in their households in adulthood, and again the effect appears stronger among those in utero (although there is evidence also for the other cohorts). This might be the case if war exposure affected women’s educational, health, and reproductive outcomes in ways that placed them in a more precarious position relative to men in the marriage market.

However, this is a subject for further study given the complexity of the potential pathways and mechanisms. The large effects measured for children who were exposed to the war in utero in particular warrant further investigation. These results are consistent with the evidence from a large literature showing that conditions and events in utero can have long-lasting consequences for the individual’s physical and mental health as well as their education, employment, and earnings outcomes (Ravelli et al 1976 ; Hoek et al 1998 ; Almond 2006 ; Dunn 2007 ; Camacho 2009 ; Almond and Currie 2011 ; Comfort 2016 ). However, much more work is needed to disentangle the biological from the social mechanisms in order to better understand both the direct and more indirect channels through which foetal-origin effects are generated (Almond and Currie 2011 ; Almond et al. 2018 ).

The relevance of our study and the need for further work in this area is underscored by the pervasiveness of domestic violence. A recent study estimated the global prevalence of intimate partner violence to be around 30%, and for the sub-Saharan African region specifically, closer to 37% (WHO 2017 ). Moreover, the consequences of domestic violence, both human and economic, are substantial. Domestic violence results in direct physical and mental harm to women, with research pointing to poorer health outcomes and a greater likelihood of depressive symptoms and substance abuse among victims (Coker et al. 2002 ; Silverman et al. 2006 ; Ackerson et al. 2008 ; Ellsberg et al. 2008 ; Meekers et al. 2013 ). Domestic violence can also result in substantial economic costs related to policing, health expenditure, and reduced economic productivity (Walby 2004 ). Lastly, children of women who experience domestic violence have worse outcomes, such as lower birth weight, lower IQ scores, a greater likelihood of emotional and behavioural problems, and a higher probability of acquiring HIV (Sternberg et al. 1993 ; Koenen et al. 2003 ; Aizer 2011 ; WHO 2013 ; Rawlings and Siddique 2014 , 2018 ; Currie et al 2022 ). Understanding both the causes and longer-term implications of domestic violence is imperative to designing appropriate policy responses and support mechanisms.

Data availability

The dataset used to obtain the results for this paper can be made available upon request.

These three main regions were subsequently demarcated into six geopolitical regions, namely the northeast, northwest, north-central, south-south, south-east, and south-west, the latter being the region where the civil war was fought (Alapiki 2005 ). These six regions are further divided into 36 states.

The 2008 Nigerian Demographic Health survey also interviewed men aged 15 to 59 to provide information on health and other related issues, but it did not collect information on their experiences of domestic violence.

We were unable to analyse exposure after age 12 (or among cohorts born pre-1958) because the DHS contains information only on women aged 15 to 49 years old. In the 2008 DHS wave, the oldest woman in the sample (aged 49) therefore was born in 1958. If we use later waves of the DHS, we can only analyse a smaller sample of war-exposed women. Specifically, if we used the 2013 DHS, we would only be able to estimate the effect for those exposed in utero to age 7, and if we used the 2018 DHS, we would only be able to estimate the effect for those exposed in utero to age 2.

The DHS captures information on experiences of domestic violence using the World Health Organization’s ethical and safety guidelines (Kishor and Kiersten 2004 ). Interviewers are trained to deal with the sensitive nature of the questions and there are strict protocols to ensure privacy during the interview. To try to minimise under-reporting of domestic violence, the DHS domestic violence questionnaire uses a modified version of the Conflict Tactics Scale (CTS). Women are asked a number of separate questions on different types of violence which reduces confusion as to what constitutes domestic violence, and gives women multiple opportunities to reveal their experiences (Kishor 2005 ).

We limit our control group to the six-year period following the war, as too broad a window of comparison increases potential confounding effects (Akresh et al 2012a ). Moreover, our results are consistent when, following Akresh et al ( 2012a ), we use an even shorter control period, namely 1970 (Nov) to 1974.

If the immediate post-war environment in the south-eastern region did not experience a full recovery, then these impacts of war exposure would be underestimated, and our findings would represent a lower-bound effect.

To validate the placebo result, we conducted further robustness checks using equal intervals of years for the treatment and control groups (1971–1974 and 1975–1978). We find statistically insignificant effects of exposure to civil war on domestic violence in these additional checks.

Akresh et al ( 2012a ) run slightly different placebo tests on ethnic group and cohort but similarly find no significant effects. They also use estimated ethnic mortality during the war instead of ethnicity itself in their regressions to test for the validity of the identification strategy and find remarkably similar results. This leads them to conclude that the strategy to use ethnicity to identify exposure “while simple, is accurate and powerful” (Akresh et al. 2012a : 275).

Because the DHS only interviews women aged 15 to 49, the oldest women included in the 2013 survey would have been born in 1964, and therefore, we can only capture war exposure from in utero through to age 7. To estimate the exposure by birth cohort, we therefore only show the results using the pooled 2008 and 2013 datasets. We did not attempt to include the 2018 DHS in the robustness checks, as the sample of war-exposed women would have shrunk even further to those women who were exposed in utero through to 2 years of age.

The DHS couple’s recode data contain information on the husbands/partners (aged 15–59) for the sample of women who were married/cohabiting and living with their partners during the interview.

The high level of intra-ethnic marriage is consistent with low levels of migration across states, with most migration in Nigeria occurring within states from rural to urban areas (Federal Office of Statistics 1999 ; 2000).

Unfortunately, we are unable to test more formally for a relationship between the intensity of conflict and domestic violence. To do so would require data on the variation in the number of deaths caused by the civil war across districts and time, and to the best of our knowledge, no such data exist (there are only estimates of the total number of deaths caused by the war).

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Department of Peace Studies and International Development, Faculty of Management, Law, and Social Sciences, University of Bradford, Bradford, UK

Joseph B. Ajefu

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Ajefu, J.B., Casale, D. Long-Term Effects of Childhood Exposure to War on Domestic Violence. Eur J Dev Res (2024). https://doi.org/10.1057/s41287-024-00659-4

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Accepted : 14 July 2024

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