essay on obesity and health

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Essay on Obesity

List of essays on obesity, essay on obesity – short essay (essay 1 – 150 words), essay on obesity (essay 2 – 250 words), essay on obesity – written in english (essay 3 – 300 words), essay on obesity – for school students (class 5, 6, 7, 8, 9, 10, 11 and 12 standard) (essay 4 – 400 words), essay on obesity – for college students (essay 5 – 500 words), essay on obesity – with causes and treatment (essay 6 – 600 words), essay on obesity – for science students (essay 7 – 750 words), essay on obesity – long essay for medical students (essay 8 – 1000 words).

Obesity is a chronic health condition in which the body fat reaches abnormal level. Obesity occurs when we consume much more amount of food than our body really needs on a daily basis. In other words, when the intake of calories is greater than the calories we burn out, it gives rise to obesity.

Audience: The below given essays are exclusively written for school students (Class 5, 6, 7, 8, 9, 10, 11 and 12 Standard), college, science and medical students.

Introduction:

Obesity means being excessively fat. A person would be said to be obese if his or her body mass index is beyond 30. Such a person has a body fat rate that is disproportionate to his body mass.

Obesity and the Body Mass Index:

The body mass index is calculated considering the weight and height of a person. Thus, it is a scientific way of determining the appropriate weight of any person. When the body mass index of a person indicates that he or she is obese, it exposes the person to make health risk.

Stopping Obesity:

There are two major ways to get the body mass index of a person to a moderate rate. The first is to maintain a strict diet. The second is to engage in regular physical exercise. These two approaches are aimed at reducing the amount of fat in the body.

Conclusion:

Obesity can lead to sudden death, heart attack, diabetes and may unwanted illnesses. Stop it by making healthy choices.

Obesity has become a big concern for the youth of today’s generation. Obesity is defined as a medical condition in which an individual gains excessive body fat. When the Body Mass Index (BMI) of a person is over 30, he/ she is termed as obese.

Obesity can be a genetic problem or a disorder that is caused due to unhealthy lifestyle habits of a person. Physical inactivity and the environment in which an individual lives, are also the factors that leads to obesity. It is also seen that when some individuals are in stress or depression, they start cultivating unhealthy eating habits which eventually leads to obesity. Medications like steroids is yet another reason for obesity.

Obesity has several serious health issues associated with it. Some of the impacts of obesity are diabetes, increase of cholesterol level, high blood pressure, etc. Social impacts of obesity includes loss of confidence in an individual, lowering of self-esteem, etc.

The risks of obesity needs to be prevented. This can be done by adopting healthy eating habits, doing some physical exercise regularly, avoiding stress, etc. Individuals should work on weight reduction in order to avoid obesity.

Obesity is indeed a health concern and needs to be prioritized. The management of obesity revolves around healthy eating habits and physical activity. Obesity, if not controlled in its initial stage can cause many severe health issues. So it is wiser to exercise daily and maintain a healthy lifestyle rather than being the victim of obesity.

Obesity can be defined as the clinical condition where accumulation of excessive fat takes place in the adipose tissue leading to worsening of health condition. Usually, the fat is deposited around the trunk and also the waist of the body or even around the periphery.

Obesity is actually a disease that has been spreading far and wide. It is preventable and certain measures are to be taken to curb it to a greater extend. Both in the developing and developed countries, obesity has been growing far and wide affecting the young and the old equally.

The alarming increase in obesity has resulted in stimulated death rate and health issues among the people. There are several methods adopted to lose weight and they include different diet types, physical activity and certain changes in the current lifestyle. Many of the companies are into minting money with the concept of inviting people to fight obesity.

In patients associated with increased risk factor related to obesity, there are certain drug therapies and other procedures adopted to lose weight. There are certain cost effective ways introduced by several companies to enable clinic-based weight loss programs.

Obesity can lead to premature death and even cause Type 2 Diabetes Mellitus. Cardiovascular diseases have also become the part and parcel of obese people. It includes stroke, hypertension, gall bladder disease, coronary heart disease and even cancers like breast cancer, prostate cancer, endometrial cancer and colon cancer. Other less severe arising due to obesity includes osteoarthritis, gastro-esophageal reflux disease and even infertility.

Hence, serious measures are to be taken to fight against this dreadful phenomenon that is spreading its wings far and wide. Giving proper education on benefits of staying fit and mindful eating is as important as curbing this issue. Utmost importance must be given to healthy eating habits right from the small age so that they follow the same until the end of their life.

Obesity is majorly a lifestyle disease attributed to the extra accumulation of fat in the body leading to negative health effects on a person. Ironically, although prevalent at a large scale in many countries, including India, it is one of the most neglect health problems. It is more often ignored even if told by the doctor that the person is obese. Only when people start acquiring other health issues such as heart disease, blood pressure or diabetes, they start taking the problem of obesity seriously.

Obesity Statistics in India:

As per a report, India happens to figure as the third country in the world with the most obese people. This should be a troubling fact for India. However, we are yet to see concrete measures being adopted by the people to remain fit.

Causes of Obesity:

Sedentary lifestyle, alcohol, junk food, medications and some diseases such as hypothyroidism are considered as the factors which lead to obesity. Even children seem to be glued to televisions, laptops and video games which have taken away the urge for physical activities from them. Adding to this, the consumption of junk food has further aggravated the growing problem of obesity in children.

In the case of adults, most of the professions of today make use of computers which again makes people sit for long hours in one place. Also, the hectic lifestyle of today makes it difficult for people to spare time for physical activities and people usually remain stressed most of the times. All this has contributed significantly to the rise of obesity in India.

Obesity and BMI:

Body Mass Index (BMI) is the measure which allows a person to calculate how to fit he or she is. In other words, the BMI tells you if you are obese or not. BMI is calculated by dividing the weight of a person in kg with the square of his / her height in metres. The number thus obtained is called the BMI. A BMI of less than 25 is considered optimal. However, if a person has a BMI over 30 he/she is termed as obese.

What is a matter of concern is that with growing urbanisation there has been a rapid increase of obese people in India? It is of utmost importance to consider this health issue a serious threat to the future of our country as a healthy body is important for a healthy soul. We should all be mindful of what we eat and what effect it has on our body. It is our utmost duty to educate not just ourselves but others as well about this serious health hazard.

Obesity can be defined as a condition (medical) that is the accumulation of body fat to an extent that the excess fat begins to have a lot of negative effects on the health of the individual. Obesity is determined by examining the body mass index (BMI) of the person. The BMI is gotten by dividing the weight of the person in kilogram by the height of the person squared.

When the BMI of a person is more than 30, the person is classified as being obese, when the BMI falls between 25 and 30, the person is said to be overweight. In a few countries in East Asia, lower values for the BMI are used. Obesity has been proven to influence the likelihood and risk of many conditions and disease, most especially diabetes of type 2, cardiovascular diseases, sleeplessness that is obstructive, depression, osteoarthritis and some cancer types.

In most cases, obesity is caused through a combination of genetic susceptibility, a lack of or inadequate physical activity, excessive intake of food. Some cases of obesity are primarily caused by mental disorder, medications, endocrine disorders or genes. There is no medical data to support the fact that people suffering from obesity eat very little but gain a lot of weight because of slower metabolism. It has been discovered that an obese person usually expends much more energy than other people as a result of the required energy that is needed to maintain a body mass that is increased.

It is very possible to prevent obesity with a combination of personal choices and social changes. The major treatments are exercising and a change in diet. We can improve the quality of our diet by reducing our consumption of foods that are energy-dense like those that are high in sugars or fat and by trying to increase our dietary fibre intake.

We can also accompany the appropriate diet with the use of medications to help in reducing appetite and decreasing the absorption of fat. If medication, exercise and diet are not yielding any positive results, surgery or gastric balloon can also be carried out to decrease the volume of the stomach and also reduce the intestines’ length which leads to the feel of the person get full early or a reduction in the ability to get and absorb different nutrients from a food.

Obesity is the leading cause of ill-health and death all over the world that is preventable. The rate of obesity in children and adults has drastically increased. In 2015, a whopping 12 percent of adults which is about 600 million and about 100 million children all around the world were found to be obese.

It has also been discovered that women are more obese than men. A lot of government and private institutions and bodies have stated that obesity is top of the list of the most difficult and serious problems of public health that we have in the world today. In the world we live today, there is a lot of stigmatisation of obese people.

We all know how troubling the problem of obesity truly is. It is mainly a form of a medical condition wherein the body tends to accumulate excessive fat which in turn has negative repercussions on the health of an individual.

Given the current lifestyle and dietary style, it has become more common than ever. More and more people are being diagnosed with obesity. Such is its prevalence that it has been termed as an epidemic in the USA. Those who suffer from obesity are at a much higher risk of diabetes, heart diseases and even cancer.

In order to gain a deeper understanding of obesity, it is important to learn what the key causes of obesity are. In a layman term, if your calorie consumption exceeds what you burn because of daily activities and exercises, it is likely to lead to obesity. It is caused over a prolonged period of time when your calorie intake keeps exceeding the calories burned.

Here are some of the key causes which are known to be the driving factors for obesity.

If your diet tends to be rich in fat and contains massive calorie intake, you are all set to suffer from obesity.

Sedentary Lifestyle:

With most people sticking to their desk jobs and living a sedentary lifestyle, the body tends to get obese easily.

Of course, the genetic framework has a lot to do with obesity. If your parents are obese, the chance of you being obese is quite high.

The weight which women gain during their pregnancy can be very hard to shed and this is often one of the top causes of obesity.

Sleep Cycle:

If you are not getting an adequate amount of sleep, it can have an impact on the hormones which might trigger hunger signals. Overall, these linked events tend to make you obese.

Hormonal Disorder:

There are several hormonal changes which are known to be direct causes of obesity. The imbalance of the thyroid stimulating hormone, for instance, is one of the key factors when it comes to obesity.

Now that we know the key causes, let us look at the possible ways by which you can handle it.

Treatment for Obesity:

As strange as it may sound, the treatment for obesity is really simple. All you need to do is follow the right diet and back it with an adequate amount of exercise. If you can succeed in doing so, it will give you the perfect head-start into your journey of getting in shape and bidding goodbye to obesity.

There are a lot of different kinds and styles of diet plans for obesity which are available. You can choose the one which you deem fit. We recommend not opting for crash dieting as it is known to have several repercussions and can make your body terribly weak.

The key here is to stick to a balanced diet which can help you retain the essential nutrients, minerals, and, vitamins and shed the unwanted fat and carbs.

Just like the diet, there are several workout plans for obesity which are available. It is upon you to find out which of the workout plan seems to be apt for you. Choose cardio exercises and dance routines like Zumba to shed the unwanted body weight. Yoga is yet another method to get rid of obesity.

So, follow a blend of these and you will be able to deal with the trouble of obesity in no time. We believe that following these tips will help you get rid of obesity and stay in shape.

Obesity and overweight is a top health concern in the world due to the impact it has on the lives of individuals. Obesity is defined as a condition in which an individual has excessive body fat and is measured using the body mass index (BMI) such that, when an individual’s BMI is above 30, he or she is termed obese. The BMI is calculated using body weight and height and it is different for all individuals.

Obesity has been determined as a risk factor for many diseases. It results from dietary habits, genetics, and lifestyle habits including physical inactivity. Obesity can be prevented so that individuals do not end up having serious complications and health problems. Chronic illnesses like diabetes, heart diseases and relate to obesity in terms of causes and complications.

Factors Influencing Obesity:

Obesity is not only as a result of lifestyle habits as most people put it. There are other important factors that influence obesity. Genetics is one of those factors. A person could be born with genes that predispose them to obesity and they will also have difficulty in losing weight because it is an inborn factor.

The environment also influences obesity because the diet is similar in certain environs. In certain environments, like school, the food available is fast foods and the chances of getting healthy foods is very low, leading to obesity. Also, physical inactivity is an environmental factor for obesity because some places have no fields or tracks where people can jog or maybe the place is very unsafe and people rarely go out to exercise.

Mental health affects the eating habits of individuals. There is a habit of stress eating when a person is depressed and it could result in overweight or obesity if the person remains unhealthy for long period of time.

The overall health of individuals also matter. If a person is unwell and is prescribed with steroids, they may end up being obese. Steroidal medications enable weight gain as a side effect.

Complications of Obesity:

Obesity is a health concern because its complications are severe. Significant social and health problems are experienced by obese people. Socially, they will be bullied and their self-esteem will be low as they will perceive themselves as unworthy.

Chronic illnesses like diabetes results from obesity. Diabetes type 2 has been directly linked to obesity. This condition involves the increased blood sugars in the body and body cells are not responding to insulin as they should. The insulin in the body could also be inadequate due to decreased production. High blood sugar concentrations result in symptoms like frequent hunger, thirst and urination. The symptoms of complicated stages of diabetes type 2 include loss of vision, renal failure and heart failure and eventually death. The importance of having a normal BMI is the ability of the body to control blood sugars.

Another complication is the heightened blood pressures. Obesity has been defined as excessive body fat. The body fat accumulates in blood vessels making them narrow. Narrow blood vessels cause the blood pressures to rise. Increased blood pressure causes the heart to start failing in its physiological functions. Heart failure is the end result in this condition of increased blood pressures.

There is a significant increase in cholesterol in blood of people who are obese. High blood cholesterol levels causes the deposition of fats in various parts of the body and organs. Deposition of fats in the heart and blood vessels result in heart diseases. There are other conditions that result from hypercholesterolemia.

Other chronic illnesses like cancer can also arise from obesity because inflammation of body cells and tissues occurs in order to store fats in obese people. This could result in abnormal growths and alteration of cell morphology. The abnormal growths could be cancerous.

Management of Obesity:

For the people at risk of developing obesity, prevention methods can be implemented. Prevention included a healthy diet and physical activity. The diet and physical activity patterns should be regular and realizable to avoid strains that could result in complications.

Some risk factors for obesity are non-modifiable for example genetics. When a person in genetically predisposed, the lifestyle modifications may be have help.

For the individuals who are already obese, they can work on weight reduction through healthy diets and physical exercises.

In conclusion, obesity is indeed a major health concern because the health complications are very serious. Factors influencing obesity are both modifiable and non-modifiable. The management of obesity revolves around diet and physical activity and so it is important to remain fit.

In olden days, obesity used to affect only adults. However, in the present time, obesity has become a worldwide problem that hits the kids as well. Let’s find out the most prevalent causes of obesity.

Factors Causing Obesity:

Obesity can be due to genetic factors. If a person’s family has a history of obesity, chances are high that he/ she would also be affected by obesity, sooner or later in life.

The second reason is having a poor lifestyle. Now, there are a variety of factors that fall under the category of poor lifestyle. An excessive diet, i.e., eating more than you need is a definite way to attain the stage of obesity. Needless to say, the extra calories are changed into fat and cause obesity.

Junk foods, fried foods, refined foods with high fats and sugar are also responsible for causing obesity in both adults and kids. Lack of physical activity prevents the burning of extra calories, again, leading us all to the path of obesity.

But sometimes, there may also be some indirect causes of obesity. The secondary reasons could be related to our mental and psychological health. Depression, anxiety, stress, and emotional troubles are well-known factors of obesity.

Physical ailments such as hypothyroidism, ovarian cysts, and diabetes often complicate the physical condition and play a massive role in abnormal weight gain.

Moreover, certain medications, such as steroids, antidepressants, and contraceptive pills, have been seen interfering with the metabolic activities of the body. As a result, the long-term use of such drugs can cause obesity. Adding to that, regular consumption of alcohol and smoking are also connected to the condition of obesity.

Harmful Effects of Obesity:

On the surface, obesity may look like a single problem. But, in reality, it is the mother of several major health issues. Obesity simply means excessive fat depositing into our body including the arteries. The drastic consequence of such high cholesterol levels shows up in the form of heart attacks and other life-threatening cardiac troubles.

The fat deposition also hampers the elasticity of the arteries. That means obesity can cause havoc in our body by altering the blood pressure to an abnormal range. And this is just the tip of the iceberg. Obesity is known to create an endless list of problems.

In extreme cases, this disorder gives birth to acute diseases like diabetes and cancer. The weight gain due to obesity puts a lot of pressure on the bones of the body, especially of the legs. This, in turn, makes our bones weak and disturbs their smooth movement. A person suffering from obesity also has higher chances of developing infertility issues and sleep troubles.

Many obese people are seen to be struggling with breathing problems too. In the chronic form, the condition can grow into asthma. The psychological effects of obesity are another serious topic. You can say that obesity and depression form a loop. The more a person is obese, the worse is his/ her depression stage.

How to Control and Treat Obesity:

The simplest and most effective way, to begin with, is changing our diet. There are two factors to consider in the diet plan. First is what and what not to eat. Second is how much to eat.

If you really want to get rid of obesity, include more and more green vegetables in your diet. Spinach, beans, kale, broccoli, cauliflower, asparagus, etc., have enough vitamins and minerals and quite low calories. Other healthier options are mushrooms, pumpkin, beetroots, and sweet potatoes, etc.

Opt for fresh fruits, especially citrus fruits, and berries. Oranges, grapes, pomegranate, pineapple, cherries, strawberries, lime, and cranberries are good for the body. They have low sugar content and are also helpful in strengthening our immune system. Eating the whole fruits is a more preferable way in comparison to gulping the fruit juices. Fruits, when eaten whole, have more fibers and less sugar.

Consuming a big bowl of salad is also great for dealing with the obesity problem. A salad that includes fibrous foods such as carrots, radish, lettuce, tomatoes, works better at satiating the hunger pangs without the risk of weight gain.

A high protein diet of eggs, fish, lean meats, etc., is an excellent choice to get rid of obesity. Take enough of omega fatty acids. Remember to drink plenty of water. Keeping yourself hydrated is a smart way to avoid overeating. Water also helps in removing the toxins and excess fat from the body.

As much as possible, avoid fats, sugars, refined flours, and oily foods to keep the weight in control. Control your portion size. Replace the three heavy meals with small and frequent meals during the day. Snacking on sugarless smoothies, dry fruits, etc., is much recommended.

Regular exercise plays an indispensable role in tackling the obesity problem. Whenever possible, walk to the market, take stairs instead of a lift. Physical activity can be in any other form. It could be a favorite hobby like swimming, cycling, lawn tennis, or light jogging.

Meditation and yoga are quite powerful practices to drive away the stress, depression and thus, obesity. But in more serious cases, meeting a physician is the most appropriate strategy. Sometimes, the right medicines and surgical procedures are necessary to control the health condition.

Obesity is spreading like an epidemic, haunting both the adults and the kids. Although genetic factors and other physical ailments play a role, the problem is mostly caused by a reckless lifestyle.

By changing our way of living, we can surely take control of our health. In other words, it would be possible to eliminate the condition of obesity from our lives completely by leading a healthy lifestyle.

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Obesity Essay

Last updated on: Feb 9, 2023

Obesity Essay: A Complete Guide and Topics

By: Nova A.

11 min read

Reviewed By: Jacklyn H.

Published on: Aug 31, 2021

Are you assigned to write an essay about obesity? The first step is to define obesity.

The obesity epidemic is a major issue facing our country right now. It's complicated- it could be genetic or due to your environment, but either way, there are ways that you can fix it!

Learn all about what causes weight gain and get tips on how you can get healthy again.

On this Page

What is Obesity

What is obesity? Obesity and BMI (body mass index) are both tools of measurement that are used by doctors to assess body fat according to the height, age, and gender of a person. If the BMI is between 25 to 29.9, that means the person has excess weight and body fat.

If the BMI exceeds 30, that means the person is obese. Obesity is a condition that increases the risk of developing cardiovascular diseases, high blood pressure, and other medical conditions like metabolic syndrome, arthritis, and even some types of cancer.

Obesity Definition

Obesity is defined by the World Health Organization as an accumulation of abnormal and excess body fat that comes with several risk factors. It is measured by the body mass index BMI, body weight (in kilograms) divided by the square of a person’s height (in meters).

Obesity in America

Obesity is on the verge of becoming an epidemic as 1 in every 3 Americans can be categorized as overweight and obese. Currently, America is an obese country, and it continues to get worse.

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Causes of obesity

Do you see any obese or overweight people around you?

You likely do.

This is because fast-food chains are becoming more and more common, people are less active, and fruits and vegetables are more expensive than processed foods, thus making them less available to the majority of society. These are the primary causes of obesity.

Obesity is a disease that affects all age groups, including children and elderly people.

Now that you are familiar with the topic of obesity, writing an essay won’t be that difficult for you.

How to Write an Obesity Essay

The format of an obesity essay is similar to writing any other essay. If you need help regarding how to write an obesity essay, it is the same as writing any other essay.

Obesity Essay Introduction

The trick is to start your essay with an interesting and catchy sentence. This will help attract the reader's attention and motivate them to read further. You don’t want to lose the reader’s interest in the beginning and leave a bad impression, especially if the reader is your teacher.

A hook sentence is usually used to open the introductory paragraph of an essay in order to make it interesting. When writing an essay on obesity, the hook sentence can be in the form of an interesting fact or statistic.

Head on to this detailed article on hook examples to get a better idea.

Once you have hooked the reader, the next step is to provide them with relevant background information about the topic. Don’t give away too much at this stage or bombard them with excess information that the reader ends up getting bored with. Only share information that is necessary for the reader to understand your topic.

Next, write a strong thesis statement at the end of your essay, be sure that your thesis identifies the purpose of your essay in a clear and concise manner. Also, keep in mind that the thesis statement should be easy to justify as the body of your essay will revolve around it.

Body Paragraphs

The details related to your topic are to be included in the body paragraphs of your essay. You can use statistics, facts, and figures related to obesity to reinforce your thesis throughout your essay.

If you are writing a cause-and-effect obesity essay, you can mention different causes of obesity and how it can affect a person’s overall health. The number of body paragraphs can increase depending on the parameters of the assignment as set forth by your instructor.

Start each body paragraph with a topic sentence that is the crux of its content. It is necessary to write an engaging topic sentence as it helps grab the reader’s interest. Check out this detailed blog on writing a topic sentence to further understand it.

End your essay with a conclusion by restating your research and tying it to your thesis statement. You can also propose possible solutions to control obesity in your conclusion. Make sure that your conclusion is short yet powerful.

Obesity Essay Examples

Essay about Obesity (PDF)

Childhood Obesity Essay (PDF)

Obesity in America Essay (PDF)

Essay about Obesity Cause and Effects (PDF)

Satire Essay on Obesity (PDF) 

Obesity Argumentative Essay (PDF)

Obesity Essay Topics

Choosing a topic might seem an overwhelming task as you may have many ideas for your assignment. Brainstorm different ideas and narrow them down to one, quality topic.

If you need some examples to help you with your essay topic related to obesity, dive into this article and choose from the list of obesity essay topics.

Childhood Obesity

As mentioned earlier, obesity can affect any age group, including children. Obesity can cause several future health problems as children age.

Here are a few topics you can choose from and discuss for your childhood obesity essay:

• What are the causes of increasing obesity in children?
• Obese parents may be at risk for having children with obesity.
• What is the ratio of obesity between adults and children?
• What are the possible treatments for obese children?
• Are there any social programs that can help children with combating obesity?
• Has technology boosted the rate of obesity in children?
• Are children spending more time on gadgets instead of playing outside?
• Schools should encourage regular exercises and sports for children.
• How can sports and other physical activities protect children from becoming obese?
• Can childhood abuse be a cause of obesity among children?
• What is the relationship between neglect in childhood and obesity in adulthood?
• Does obesity have any effect on the psychological condition and well-being of a child?
• Are electronic medical records effective in diagnosing obesity among children?
• Obesity can affect the academic performance of your child.
• Do you believe that children who are raised by a single parent can be vulnerable to obesity?
• You can promote interesting exercises to encourage children.
• What is the main cause of obesity, and why is it increasing with every passing day?
• Schools and colleges should work harder to develop methodologies to decrease childhood obesity.
• The government should not allow schools and colleges to include sweet or fatty snacks as a part of their lunch.
• If a mother is obese, can it affect the health of the child?
• Children who gain weight frequently can develop chronic diseases.

Obesity Argumentative Essay Topics

Do you want to write an argumentative essay on the topic of obesity?

The following list can help you with that!

Here are some examples you can choose from for your argumentative essay about obesity:

• Can vegetables and fruits decrease the chances of obesity?
• Should you go for surgery to overcome obesity?
• Are there any harmful side effects?
• Can obesity be related to the mental condition of an individual?
• Are parents responsible for controlling obesity in childhood?
• What are the most effective measures to prevent the increase in the obesity rate?
• Why is the obesity rate increasing in the United States?
• Can the lifestyle of a person be a cause of obesity?
• Does the economic situation of a country affect the obesity rate?
• How is obesity considered an international health issue?
• Can technology and gadgets affect obesity rates?
• What can be the possible reasons for obesity in a school?
• How can we address the issue of obesity?
• Is obesity a chronic disease?
• Is obesity a major cause of heart attacks?
• Are the junk food chains causing an increase in obesity?
• Do nutritional programs help in reducing the obesity rate?
• How can the right type of diet help with obesity?
• Why should we encourage sports activities in schools and colleges?
• Can obesity affect a person’s behavior?

Health Related Topics for Research Paper

If you are writing a research paper, you can explain the cause and effect of obesity.

Here are a few topics that link to the cause and effects of obesity.Review the literature of previous articles related to obesity. Describe the ideas presented in the previous papers.

• Can family history cause obesity in future generations?
• Can we predict obesity through genetic testing?
• What is the cause of the increasing obesity rate?
• Do you think the increase in fast-food restaurants is a cause of the rising obesity rate?
• Is the ratio of obese women greater than obese men?
• Why are women more prone to be obese as compared to men?
• Stress can be a cause of obesity. Mention the reasons how mental health can be related to physical health.
• Is urban life a cause of the increasing obesity rate?
• People from cities are prone to be obese as compared to people from the countryside.
• How obesity affects the life expectancy of people? What are possible solutions to decrease the obesity rate?
• Do family eating habits affect or trigger obesity?
• How do eating habits affect the health of an individual?
• How can obesity affect the future of a child?
• Obese children are more prone to get bullied in high school and college.
• Why should schools encourage more sports and exercise for children?

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Topics for Essay on Obesity as a Problem

Do you think a rise in obesity rate can affect the economy of a country?

Here are some topics for your assistance regarding your economics related obesity essay.

• Does socioeconomic status affect the possibility of obesity in an individual?
• Analyze the film and write a review on “Fed Up” – an obesity epidemic.
• Share your reviews on the movie “The Weight of The Nation.”
• Should we increase the prices of fast food and decrease the prices of fruits and vegetables to decrease obesity?
• Do you think healthy food prices can be a cause of obesity?
• Describe what measures other countries have taken in order to control obesity?
• The government should play an important role in controlling obesity. What precautions should they take?
• Do you think obesity can be one of the reasons children get bullied?
• Do obese people experience any sort of discrimination or inappropriate behavior due to their weight?
• Are there any legal protections for people who suffer from discrimination due to their weight?
• Which communities have a higher percentage of obesity in the United States?
• Discuss the side effects of the fast-food industry and their advertisements on children.
• Describe how the increasing obesity rate has affected the economic condition of the United States.
• What is the current percentage of obesity all over the world? Is the obesity rate increasing with every passing day?
• Why is the obesity rate higher in the United States as compared to other countries?
• Do Asians have a greater percentage of obese people as compared to Europe?
• Does the cultural difference affect the eating habits of an individual?
• Obesity and body shaming.
• Why is a skinny body considered to be ideal? Is it an effective way to reduce the obesity rate?

Obesity Solution Essay Topics

With all the developments in medicine and technology, we still don’t have exact measures to treat obesity.

Here are some insights you can discuss in your essay:

• How do obese people suffer from metabolic complications?
• Describe the fat distribution in obese people.
• Is type 2 diabetes related to obesity?
• Are obese people more prone to suffer from diabetes in the future?
• How are cardiac diseases related to obesity?
• Can obesity affect a woman’s childbearing time phase?
• Describe the digestive diseases related to obesity.
• Obesity may be genetic.
• Obesity can cause a higher risk of suffering a heart attack.
• What are the causes of obesity? What health problems can be caused if an individual suffers from obesity?
• What are the side effects of surgery to overcome obesity?
• Which drugs are effective when it comes to the treatment of obesity?
• Is there a difference between being obese and overweight?
• Can obesity affect the sociological perspective of an individual?
• Explain how an obesity treatment works.
• How can the government help people to lose weight and improve public health?

Writing an essay is a challenging yet rewarding task. All you need is to be organized and clear when it comes to academic writing.

• Choose a topic you would like to write on.
• Organize your thoughts.
• Pen down your ideas.
• Compose a perfect essay that will help you ace your subject.
• Proofread and revise your paper.

Were the topics useful for you? We hope so!

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As a Digital Content Strategist, Nova Allison has eight years of experience in writing both technical and scientific content. With a focus on developing online content plans that engage audiences, Nova strives to write pieces that are not only informative but captivating as well.

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Health Effects of Overweight and Obesity

Obesity and Excess Weight Increase Risk of Severe Illness; Racial and Ethnic Disparities Persist

Food Assistance and Food Systems Resources

People who have overweight or obesity*, compared to those with healthy weight, are at increased risk for many serious diseases and health conditions. These include: 1,2,3

• All-causes of death (mortality).
• High blood pressure (hypertension).
• High LDL cholesterol, low HDL cholesterol, or high levels of triglycerides (dyslipidemia).
• Type 2 diabetes.
• Coronary heart disease.
• Gallbladder disease.
• Osteoarthritis (a breakdown of cartilage and bone within a joint).
• Sleep apnea and breathing problems.
• Many types of cancer .
• Low quality of life.
• Mental illness such as clinical depression, anxiety, and other mental disorders 4,5.
• Body pain and difficulty with physical functioning 6.

*Overweight is defined as a body mass index (BMI) of 25 or higher. Obesity is defined as a BMI of 30 or higher. See the BMI calculator for people 20 years and older and the BMI calculator for people ages 2 through 19 .

Overweight and Obesity Data, strategies, and initiatives—CDC.

Weight Loss for Good Being overweight brings added risks for people with diabetes—American Diabetes Association.

Clinical Guidelines on the Identification, Evaluation, And Treatment of Overweight And Obesity in Adults [PDF-1.28MB] Health problems associated with overweight and obesity—National Heart, Lung and Blood Institute.

Health Risks of Overweight and Obesity Causes, risk factors, screening, prevention and more—National Heart, Lung and Blood Institute.

Adult Obesity Maps Self-reported US adult obesity prevalence by race, ethnicity, and location.

1 NHLBI. 2013. Managing Overweight and Obesity in Adults: Systematic Evidence Review from the Obesity Expert Panel. [PDF-5.89MB]

2 Clinical Guidelines on the Identification, Evaluation, and Treatment of Overweight and Obesity in Adults. [PDF-1.25MB]

3 Bhaskaran K, Douglas I, Forbes H, dos-Santos-Silva I, Leon DA, Smeeth L. Body-mass index and risk of 22 specific cancers: a population-based cohort study of 5•24 million UK adults. Lancet . 2014 Aug 30;384(9945):755-65.

4 Kasen, Stephanie, et al. “Obesity and psychopathology in women: a three decade prospective study.” International Journal of Obesity 32.3 (2008): 558-566.

5 Luppino, Floriana S., et al. “Overweight, obesity, and depression: a systematic review and meta-analysis of longitudinal studies. “ Archives of General Psychiatry 67.3 (2010): 220-229.

6 Roberts, Robert E., et al. “Prospective association between obesity and depression: evidence from the Alameda County Study.” International Journal of Obesity 27.4 (2003): 514-521.

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Essay on Obesity

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

Let’s take a look…

100 Words Essay on Obesity

Understanding obesity.

Obesity is a health condition where a person has excess body fat. It’s often measured using the Body Mass Index (BMI).

Causes of Obesity

Obesity can be caused by eating too much and not exercising enough. Also, genetics and lifestyle can play a role.

Effects of Obesity

Obesity can lead to serious health problems like heart disease, diabetes, and certain types of cancer.

Preventing Obesity

Eating a balanced diet and regular physical activity can help prevent obesity. It’s important to maintain a healthy lifestyle.

Also check:

• Paragraph on Obesity
• Speech on Obesity

250 Words Essay on Obesity

Introduction.

Obesity represents a significant public health issue worldwide, posing detrimental effects to physical health and psychological well-being. It is a complex disorder involving an excessive amount of body fat, often resulting from a combination of genetic, behavioral, and environmental factors.

The primary cause of obesity is an energy imbalance between calories consumed and expended. This disparity is often fueled by unhealthy diets rich in fats and sugars, and a sedentary lifestyle. Genetics also play a critical role, affecting how the body metabolizes food and stores fat.

Implications on Health

Obesity significantly increases the risk of various diseases, including heart disease, diabetes, and certain cancers. Additionally, it can lead to mental health issues like depression and lower quality of life.

Prevention and Management

Preventing obesity requires a multi-faceted approach. It entails adopting a healthier diet, increasing physical activity, and creating supportive environments that promote healthy choices. Management of obesity often involves similar strategies, though in some cases, medication or surgery may be necessary.

In conclusion, obesity is a pressing global health concern that requires immediate attention. It is crucial to promote healthier lifestyles and create supportive environments to combat this epidemic. The battle against obesity is not only about individual responsibility but also about societal commitment to fostering healthful living.

500 Words Essay on Obesity

Obesity, a complex and multifaceted health issue, has become a global epidemic. Characterized by excessive body fat, it poses a significant risk to an individual’s health, leading to numerous chronic illnesses. This essay will delve into the causes, consequences, and potential solutions to this growing health crisis.

The primary cause of obesity is an energy imbalance between calories consumed and expended. This is often due to a combination of excessive dietary intake, lack of physical activity, and genetic susceptibility. However, it is important to recognize the role of socio-economic factors. The availability of high-calorie, low-nutrient food, urbanization, and sedentary lifestyles have all contributed to the rise in obesity rates.

Health Consequences

Obesity significantly increases the risk of various health problems. It is a major risk factor for noncommunicable diseases (NCDs) such as cardiovascular diseases, diabetes, musculoskeletal disorders, and some cancers. Moreover, obesity can lead to psychological issues, including depression, anxiety, and low self-esteem.

Socioeconomic Impact

The socioeconomic impact of obesity is profound. It places a heavy burden on healthcare systems due to the high cost of treating obesity-related diseases. Furthermore, obesity can lead to reduced productivity and increased absenteeism in the workforce, affecting economic growth.

Prevention and Control

Preventing and controlling obesity requires a multifaceted approach. At the individual level, this includes adopting a healthy diet and regular physical activity. However, individual behavior is shaped by the broader socio-environmental context. Therefore, public health interventions are crucial. These may include policies to regulate food advertising, promote active transportation, and ensure access to affordable, nutritious food.

In conclusion, obesity is a complex issue with far-reaching consequences. It is driven by a combination of individual, environmental, and socio-economic factors. Therefore, addressing this problem requires concerted efforts at multiple levels. By implementing comprehensive strategies that promote healthy lifestyles and create supportive environments, we can combat the obesity epidemic and improve public health.

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• Essay on Nutrition
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• Essay on Nuclear Energy

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Essay on Obesity

Introduction

Obesity is a health condition that frequently develops when an individual’s weight is out of proportion to their height and age. It is critical to help obese individuals with their lifestyle choices, as they are frequently abused and ignored emotionally and physically by family members and friends. Additionally, obesity rates are increasing, and obesity can frequently obstruct individuals’ growth and even result in significant psychological issues resulting from continual criticism and rejection (Psalios, 2020). Obesity has long been a source of contention among psychologists, sociologists, and dietitians worldwide. Numerous factors have been and continue to be studied from a practical and theoretical standpoint, including race, heredity, behavior, environment, gender, and other socioeconomic circumstances. Nevertheless, obesity remains a hot subject nowadays, and in some situations, the causes and consequences of obesity are complex and difficult to decipher.

Risk of health problems related to obesity

People have not been sufficiently informed about the high addictiveness of food and associated health risks. Individuals increasingly lack knowledge about their condition, critical lifestyle changes, and critical self-management skills. In any event, it should be noted that obesity is a significant issue, which impacts the individual and the community, and society as a whole. However, when individuals are obese, they might jeopardize the future of every person involved.

Obesity is a result of an individual’s genetics, upbringing, and socioeconomic situation and may dramatically influence individuals’ general health and wellness. It is commonly defined by a 30percent excess of body fat over an individual’s optimum age and height. However, there are numerous factors, which contribute to an individual being overweight. One of the primary reasons an individual may struggle with their weight is that they are genetically prone and at a higher risk of being overweight or having other severe illnesses and diseases due to a biological family member carrying the gene. Genetic factors and human hormones contribute significantly to the genesis of obesity (Qasim et al., 2018).

Individuals assume they can prevent or reverse obesity before it causes health concerns. The fact is that most individuals would be unable to overcome obesity, and nearly half may die as a result of obesity-related diseases. Most obese individuals are unaware that obesity also causes difficulty in breathing, early symptoms of cardiac disease, disturbed sleep patterns, surgical complications, nonalcoholic fatty liver disease, polycystic ovarian syndrome, and type II diabetes. Obesity may also cause high blood pressure. Individuals who are overweight are more likely to get high blood pressure. The cause is high blood fat content (triglycerides) and low HDL good cholesterol in the blood of obese persons. Triglycerides can cause blood vessels to clog quickly. When the space of the blood vessels has narrowed, then the pressure in them will increase.

Obese people have a higher risk of various types of cancer, such as endometrial cancer, namely cancer of the lining of the colon, uterus, kidney, prostate, gall bladder, and post-menopausal and breast cancer. In addition, for every 2-pound increase in weight, the risk of developing arthritis is increased by 9 to 13%. Knowing that arthritis can be increased with weight loss is prevalent for the betterment of the individual.

Obesity can harm the knees and hips because the extra weight puts strain on the joints. While joint replacement surgery is commonly performed on injured joints, the artificial joint has a higher risk of slackening and causing more damage. The effects of Obesity could also raise the risk of vitamin deficiencies (vitamin B12) that can lead to bone and joint issues (like sliding bow legs and femoral epiphysis) and other mental illnesses like low self-esteem and depression (Thomas-Valdés et al., 2017).

Obesity can also contribute to poor mental well-being, social discrimination, unfavorable peer/adult relationships, high-risk behavior (use of alcohol/drug), decreased hopes for a promising future, and being misinterpreted by relatives. A person who is obese also impacts unstable emotions and often considers himself unattractive, lacks self-confidence, and suffers from depression or stress due to not being able to face a normal and active life like other individuals. Most obese people generally lack self-confidence due to their physical appearance. They continuously compare themselves against individuals with healthier figures, negatively affecting their daily lives, work performance, and social interactions.

Considering obesity impacts every organ system in the body, it may reduce life span by 2 to 5 years (Wilhelmi de Toledo et al., 2020).In addition, obesity also affects mental health. These mental effects have not been extensively studied as side effects of physical obesity. Nevertheless, evidence shows that negative obesity can also affect mental health. Feelings of inferiority are common among people whose obesity persists. Rates of depression and anxiety are more alarming because a study in Sweden found that individuals who are severely obese are three to four times more likely to exhibit signs of depression and anxiety than those with an ideal weight.

During pregnancy, obesity is connected with a higher death risk in both the mother and the baby and an increase in the risk of maternal high blood pressure (Catalano & Shankar, 2017). Women who are obese during pregnancy are likely to develop gestational diabetes and issues with labor and delivery, among other concerns. Obesity and overweight are linked to an increased risk of gallbladder disease, surgical risk, incontinence, and depression. Obesity can reduce a person’s quality of life by limiting mobility and physical strength through social, academic, and work discrimination. Also, they are obese, barriers to the quality of life, and emotional consequences seen in this disease. All these negative attributes of such disease are reduced if they were to occur to better the person.

Obesity is sometimes misunderstood as a personal issue. Even though many aspects overlap, experts appear to concur that obesity is a highly complex issue. In addition to knowing the causes of obesity, it is critical to consider ways to avoid obesity and how the community could support and assist in rehabilitating those who have such a condition. In order to combat obesity, society should employ a combination of prevention, intervention, and suppression methods. In order to be efficient, obesity prevention efforts should involve not just a healthy diet, regular exercise, and instilling good habits in everyone, but also a wide range of management tools, possible medicines, and other therapies.

Psalios, S. (2020).  Collateral Damage of the ‘War on Obesity’: The Australian Anti-Obesity Campaign: From Fat Stigma to Eating Disorders  (Doctoral dissertation, La Trobe).

Qasim, A., Turcotte, M., De Souza, R. J., Samaan, M. C., Champredon, D., Dushoff, J., … & Meyre, D. (2018). On the origin of obesity: identifying the biological, environmental and cultural drivers of genetic risk among human populations.  Obesity reviews ,  19 (2), 121-149.

Thomas-Valdés, S., Tostes, M. D. G. V., Anunciação, P. C., da Silva, B. P., & Sant’Ana, H. M. P. (2017). Association between vitamin deficiency and metabolic disorders related to obesity.  Critical reviews in food science and nutrition ,  57 (15), 3332-3343.

Wilhelmi de Toledo, F., Grundler, F., Sirtori, C. R., & Ruscica, M. (2020). Unravelling the health effects of fasting: a long road from obesity treatment to healthy life span increase and improved cognition.  Annals of Medicine ,  52 (5), 147-161.

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Guest Essay

A Year on Ozempic Taught Me We’re Thinking About Obesity All Wrong

By Johann Hari

Mr. Hari is a British journalist and the author of “Magic Pill: The Extraordinary Benefits — and Disturbing Risks — of the New Weight Loss Drugs.”

Ever since I was a teenager, I have dreamed of shedding a lot of weight. So when I shrank from 203 pounds to 161 in a year, I was baffled by my feelings. I was taking Ozempic, and I was haunted by the sense that I was cheating and doing something immoral.

I’m not the only one. In the United States (where I now split my time), over 70 percent of people are overweight or obese, and according to one poll, 47 percent of respondents said they were willing to pay to take the new weight-loss drugs. It’s not hard to see why. They cause users to lose an average of 10 to 20 percent of their body weight, and clinical trials suggest that the next generation of drugs (probably available soon) leads to a 24 percent loss, on average. Yet as more and more people take drugs like Ozempic, Wegovy and Mounjaro, we get more confused as a culture, bombarding anyone in the public eye who takes them with brutal shaming.

This is happening because we are trapped in a set of old stories about what obesity is and the morally acceptable ways to overcome it. But the fact that so many of us are turning to the new weight-loss drugs can be an opportunity to find a way out of that trap of shame and stigma — and to a more truthful story.

In my lifetime, obesity has exploded, from being rare to almost being the norm. I was born in 1979, and by the time I was 21, obesity rates in the United States had more than doubled . They have skyrocketed since. The obvious question is, why? And how do these new weight-loss drugs work? The answer to both lies in one word: satiety. It’s a concept that we don’t use much in everyday life but that we’ve all experienced at some point. It describes the sensation of having had enough and not wanting any more.

The primary reason we have gained weight at a pace unprecedented in human history is that our diets have radically changed in ways that have deeply undermined our ability to feel sated. My father grew up in a village in the Swiss mountains, where he ate fresh, whole foods that had been cooked from scratch and prepared on the day they were eaten. But in the 30 years between his childhood and mine, in the suburbs of London, the nature of food transformed across the Western world. He was horrified to see that almost everything I ate was reheated and heavily processed. The evidence is clear that the kind of food my father grew up eating quickly makes you feel full. But the kind of food I grew up eating, much of which is made in factories, often with artificial chemicals, left me feeling empty and as if I had a hole in my stomach. In a recent study of what American children eat, ultraprocessed food was found to make up 67 percent of their daily diet. This kind of food makes you want to eat more and more. Satiety comes late, if at all.

One scientific experiment — which I have nicknamed Cheesecake Park — seemed to me to crystallize this effect. Paul Kenny, a neuroscientist at Mount Sinai Hospital in New York, grew up in Ireland. After he moved in 2000 to the United States in his 20s, he gained 30 pounds in two years. He began to wonder if the American diet has some kind of strange effect on our brains and our cravings, so he designed an experiment to test it. He and his colleague Paul Johnson raised a group of rats in a cage and gave them an abundant supply of healthy, balanced rat chow made out of the kind of food rats had been eating for a very long time. The rats would eat it when they were hungry, and then they seemed to feel sated and stopped. They did not become fat.

But then Dr. Kenny and his colleague exposed the rats to an American diet: fried bacon, Snickers bars, cheesecake and other treats. They went crazy for it. The rats would hurl themselves into the cheesecake, gorge themselves and emerge with their faces and whiskers totally slicked with it. They quickly lost almost all interest in the healthy food, and the restraint they used to show around healthy food disappeared. Within six weeks, their obesity rates soared.

After this change, Dr. Kenny and his colleague tweaked the experiment again (in a way that seems cruel to me, a former KFC addict). They took all the processed food away and gave the rats their old healthy diet. Dr. Kenny was confident that they would eat more of it, proving that processed food had expanded their appetites. But something stranger happened. It was as though the rats no longer recognized healthy food as food at all, and they barely ate it. Only when they were starving did they reluctantly start to consume it again.

Though Dr. Kenny’s study was in rats, we can see forms of this behavior everywhere. We are all living in Cheesecake Park — and the satiety-stealing effect of industrially assembled food is evidently what has created the need for these medications. Drugs like Ozempic work precisely by making us feel full. Carel le Roux, a scientist whose research was important to the development of these drugs, says they boost what he and others once called “satiety hormones.”

Once you understand this context, it becomes clear that processed and ultraprocessed food create a raging hole of hunger, and these treatments can repair that hole. Michael Lowe, a professor of psychology at Drexel University who has studied hunger for 40 years, told me the drugs are “an artificial solution to an artificial problem.”

Yet we have reacted to this crisis largely caused by the food industry as if it were caused only by individual moral dereliction. I felt like a failure for being fat and was furious with myself for it. Why do we turn our anger inward and not outward at the main cause of the crisis? And by extension, why do we seek to shame people taking Ozempic but not those who, say, take drugs to lower their blood pressure?

The answer, I think, lies in two very old notions. The first is the belief that obesity is a sin. When Pope Gregory I laid out the seven deadly sins in the sixth century, one of them was gluttony, usually illustrated with grotesque-seeming images of overweight people. Sin requires punishment before you can get to redemption. Think about the competition show “The Biggest Loser,” on which obese people starve and perform extreme forms of exercise in visible agony in order to demonstrate their repentance.

The second idea is that we are all in a competition when it comes to weight. Ours is a society full of people fighting against the forces in our food that are making us fatter. It is often painful to do this: You have to tolerate hunger or engage in extreme forms of exercise. It feels like a contest in which each thin person creates additional pressure on others to do the same. Looked at in this way, people on Ozempic can resemble cyclists like Lance Armstrong who used performance-enhancing drugs. Those who manage their weight without drugs might think, “I worked hard for this, and you get it for as little as a weekly jab?”

We can’t find our way to a sane, nontoxic conversation about obesity or Ozempic until we bring these rarely spoken thoughts into the open and reckon with them. You’re not a sinner for gaining weight. You’re a typical product of a dysfunctional environment that makes it very hard to feel full. If you are angry about these drugs, remember the competition isn’t between you and your neighbor who’s on weight-loss drugs. It’s between you and a food industry constantly designing new ways to undermine your satiety. If anyone is the cheat here, it’s that industry. We should be united in a struggle against it and its products, not against desperate people trying to find a way out of this trap.

There are extraordinary benefits as well as disturbing risks associated with weight-loss drugs. Reducing or reversing obesity hugely boosts health, on average: We know from years of studying bariatric surgery that it slashes the risks of cancer, heart disease and diabetes-related death. Early indications are that the new anti-obesity drugs are moving people in a similar radically healthier direction, massively reducing the risk of heart attack or stroke. But these drugs may increase the risk for thyroid cancer. I am worried they diminish muscle mass and fear they may supercharge eating disorders. This is a complex picture in which the evidence has to be weighed very carefully.

But we can’t do that if we remain lost in stories inherited from premodern popes or in a senseless competition that leaves us all, in the end, losers. Do we want these weight loss drugs to be another opportunity to tear one another down? Or do we want to realize that the food industry has profoundly altered the appetites of us all — leaving us trapped in the same cage, scrambling to find a way out?

Johann Hari is a British journalist and the author of “Magic Pill: The Extraordinary Benefits — and Disturbing Risks — of the New Weight Loss Drugs,” among other books.

Source photographs by seamartini, The Washington Post, and Zana Munteanu via Getty Images.

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Obesity in children is rising dramatically, and it comes with major – and sometimes lifelong – health consequences

2023 California Health Equity Fellow, University of Southern California

Disclosure statement

Christine Nguyen does not work for, consult, own shares in or receive funding from any company or organisation that would benefit from this article, and has disclosed no relevant affiliations beyond their academic appointment.

University of Southern California provides funding as a member of The Conversation US.

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• Bahasa Indonesia

In the past two decades, children have become more obese and have developed obesity at a younger age. A 2020 report found that 14.7 million children and adolescents in the U.S. live with obesity.

Because obesity is a known risk factor for serious health problems , its rapid increase during the COVID-19 pandemic raised alarms.

Without intervention, many obese adolescents will remain obese as adults. Even before adulthood, some children will have serious health problems beginning in their preteen years.

To address these issues, in early 2023, the American Academy of Pediatrics released its first new obesity management guidelines in 15 years.

I am a pediatric gastroenterologist who sees children in the largest public hospital in California, and I have witnessed a clear trend over the last two decades. Early in my practice, I only occasionally saw a child with a complication of obesity; now I see multiple referrals each month. Some of these children have severe obesity and several health complications that require multiple specialists.

These observations prompted my reporting for the California Health Equity Fellowship at the University of Southern California.

It’s important to note that not all children who carry extra weight are unhealthy. But evidence supports that obesity, especially severe obesity, requires further assessment.

How obesity is measured

The World Health Organization defines obesity as “abnormal or excessive fat accumulation that presents a risk to health.”

Measuring fat composition requires specialized equipment that is not available in a regular doctor’s office. Therefore most clinicians use body measurements to screen for obesity.

One method is body mass index, or BMI, a calculation based on a child’s height and weight compared to age- and sex-matched peers. BMI doesn’t measure body fat, but when BMI is high , it correlates with total body fat.

According to the American Academy of Pediatrics , a child qualifies as overweight at a BMI between the 85th and 95th percentile . Obese is defined as a BMI above the 95th percentile . Other screens for obesity include waist circumference and skin-fold thickness , but these methods are less common.

Because many children exceeded the limits of existing growth charts, in 2022 the Centers for Disease Control and Prevention introduced extended growth charts for severe obesity. Severe obesity occurs when a child reaches the 120th percentile or has a BMI over 35. For instance, a 6-year-old boy who is 48 inches tall and is 110 pounds would meet criteria for severe obesity because his BMI is 139th percentile.

Severe obesity carries a heightened risk of liver disease, cardiovascular disease and metabolic problems such as diabetes. As of 2016, almost 8% of children ages 2 to 19 had severe obesity .

Other health problems associated with severe obesity include obstructive sleep apnea , bone and joint problems that can cause early arthritis, high blood pressure and kidney disease . Many of these problems occur together.

How obesity affects the liver

The liver disease associated with obesity is called nonalcoholic fatty liver disease . To store excess dietary fat and sugar, the liver’s cells fill with fat. Excess carbohydrates in particular get processed into substances similar to the breakdown products of alcohols . Under the microscope, a pediatric fatty liver looks similar to a liver with alcohol damage.

Occasionally children with fatty liver are not obese; however, the greatest risk factor for fatty liver is obesity. At the same BMI, Hispanic and Asian children are more susceptible to fatty liver disease than Black and white children. Weight reduction or reducing the consumption of fructose, a naturally occurring sugar and common food additive – even without significant weight loss – improves fatty liver.

Fatty liver is the most common chronic liver disease in children and adults. In Southern California, pediatric fatty liver doubled from 2009 to 2018. The disease can progress rapidly in children, and some will have liver scarring after only a few years.

Although few children currently require liver transplants for fatty liver, it is the most rapidly increasing reason for transplantation in young adults . Fatty liver is the second-most common reason for liver transplantation in the U.S., and it will be the leading cause in the future .

Links between obesity and diabetes

Fatty liver is implicated in metabolic syndrome , a group of conditions that cluster together and increase the risk of cardiovascular disease and diabetes.

In a telephone interview, Dr. Barry Reiner, a pediatric endocrinologist, voiced his concerns to me about obesity and diabetes.

“When I started my practice, I had never heard of type 2 diabetes in children,” says Reiner. “Now, depending on which part of the U.S., between a quarter and a third of new cases of diabetes are type 2.”

Type 1 diabetes is an autoimmune disease previously called juvenile-onset diabetes. Conversely, type 2 diabetes was historically considered an adult disease.

However, type 2 diabetes is increasing in children, and obesity is the major risk factor . While both types of diabetes have genetic and lifestyle influences, type 2 is more modifiable through diet and exercise.

By 2060, the number of people under 20 with type 2 diabetes will increase by 700% . Black, Latino, Asian, Pacific Islander and Native American/Alaska Native children will have more type 2 diabetes diagnoses than white children.

“The seriousness of type 2 diabetes in children is underestimated,” says Reiner. He added that many people express a misconception that type 2 diabetes is a mild, slow-moving disease.

Reiner pointed to an important study showing that type 2 diabetes acquired in childhood can rapidly progress . As early as 10 to 12 years after their childhood diagnosis, patients developed nerve damage, kidney problems and vision damage. By 15 years after diagnosis, at an average age of 27, almost 70% of the patients had high blood pressure .

Most patients had more than one complication. Although rare, a few patients experienced heart attacks and strokes. When people with childhood onset diabetes became pregnant, 24% delivered premature infants, over double the rate in the general population .

Heart health

Cardiovascular changes associated with obesity and severe obesity can also increase a child’s lifetime chance of heart attacks and strokes. Carrying extra weight at 6 to 7 years old can result in higher blood pressure, cholesterol and artery stiffness by 11 to 12 years of age . Obesity changes the structure of the heart , making the muscle thicken and expand.

Although still uncommon, more people in their 20s, 30s and 40s are having strokes and heart attacks than a few decades ago. Although many factors may contribute to heart attack and stroke, obesity adds to that risk.

Talk about being healthy, not focusing on weight

Venus Kalami, a registered dietitian, spoke with me about the environmental and societal influences on childhood obesity.

“Food, diet, lifestyle and weight are often a proxy for something greater going on in someone’s life,” says Kalami.

Factors beyond a child’s control, including depression , access to healthy food and walkable neighborhoods , contribute to obesity.

Parents may wonder how to help children without introducing shame or blame. First, conversations about weight and food should be age appropriate.

“A 6-year-old does not need to be thinking about their weight,” says Kalami. She adds that even preteens and teenagers should not be focusing on their weight, though they likely already are.

Even “good-natured” teasing is harmful. Avoid diet talk, and instead discuss health. Kalami recommends that adults explain how healthy habits can improve mood, focus or kids’ performance in a favorite activity.

“A 12-year-old isn’t always going to know what is healthy,” Kalami said. “Help them pick what’s available and make the best choice, which may not be the perfect choice.”

Any weight talk, either criticism or compliments for weight loss, may backfire, she adds. Praising a child for their weight loss can reinforce a negative cycle of disordered eating. Instead, cheer the child’s better health and good choices.

Dr. Muneeza Mirza, a pediatrician, recommends that parents model healthful behavior.

“Changes should be made for the whole family,” says Mirza. “It shouldn’t be considered a punishment for that kid.”

• Cardiovascular disease
• Kidney disease
• Cardiovascular health
• Obesity epidemic
• High blood pressure
• World Health Organization (WHO)
• American Academy of Pediatrics
• Centers for Disease Control and Prevention (CDC)
• Body mass index
• Weight stigma

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Obesity as a Worldwide Problem and Its Solution Essay

Introduction, what exactly is obesity, reasons of obesity, healthy eating habits – the only solution, survey page.

The progress of a nation solely rests on the citizens. Of greater significance are their socio-economic, political conditions. A huge sum is spent every year by the government for the welfare of the subjects. With the change in policies every year, a novel decision is taken up. These decisions cater to individual interests in the larger interest of society in general.

Unfortunately, the world now witnesses an unhealthy scenario caused due to socio-economic, political imbalances. They affect the physical and mental health of individuals. Perhaps, one of the most glaring problems of the day seems to be obesity. Once, considered a symbol of wealth and social status, physical attractiveness, strength, and fertility by certain European cultures, western culture takes a negative stand on it. The obese are unattractive and negative stereotypes. They are a social stigma, targets of bullies, and shunned by peers. Above all, obesity is seen as a sign of lower socioeconomic status, more a medical condition in modern western culture. Ironically, the USA accounts for 64.5% of its population either overweight or obese.

The Times America has reported, “It’s not healthy to be obese, and if we keep going the way we are headed, the long-term medical costs may be more than we can bear” (Americas Obesity Crisis, 2004).

The problem of obesity is a worldwide issue that needs due attention. It has been medically proved that obesity could be fatal. What exactly is obesity? “The natural energy reserve, stored in the fatty tissue of human and other mammals is increased to a point where it is associated with certain health conditions or increased mortality. It is viewed as a serious and growing health problem which gives birth to certain other diseases like cardiovascular diseases, diabetes mellitus type 2, sleep apnea and osteoarthritis” (Obesity, 2008).

Visit: www win.niddk.gov/publications/health_risks.htm# sleep for more information on the relationship between sleep apnea and obesity.

BMI (body mass index) is a widely used method for estimating body fat. Calculated by dividing the subject’s weight by the square of his/her height, typically expressed either in metric or US “Customary” units, a frightening score could take away the cheer from every face.

The dreaded physical condition has umpteen reasons for its attack, the main being a sedentary lifestyle. The last quarter of the 20th century has witnessed a rapid acceleration of obesity in western society. Hence, it remains a persistent problem.

To arrive at a definite reason for a large number of obese in a nation, it would be sufficient to note the patterns of lifestyles of each individual. It would also suffice if the socio-economic conditions are taken into consideration. It would be wise to elaborate on the principal causes of this condition and arrive at a suitable solution to it.

The primary reason is we have seen earlier is an increasingly sedentary lifestyle and lack of activity. This causes the deposits of excess fat principally in the abdomen areas and hence enlargements of muscles concerned. Yet another reason could be the lower relative cost of foodstuffs. This enables people of all walks of life to take in food whether necessary or unnecessary. Increased marketing, accounts for the innumerable stock of junk food, preferred by children and adults alike. In two-income households, the clock never ticks in the kitchen, the occupants never bother to take care of their health. Food is often taken from restaurants where delicious and sumptuous food three or more times a day causes unhealthy eating habits.

Regular exercise and eating right are considered to be the best solution to the problem. Exercise requires energy (calories) stored as body fat. The body breaks down its fat stored to provide energy during prolonged aerobic exercise. Medical help ranging from pills to surgery is recommended in certain extreme cases of obesity. The probable reasons could be thyroid malfunction or other organ dysfunction.

It is the only problem that needs immediate remedy as the sufferers not only undergo physical torture but also mental anguish. In the years to come, a significant number of Americans could turn against themselves and the results could lead to disaster and deaths. I could sound embarrassing. But there is enough evidence to prove that the silent sufferers end up taking their own lives due to social pressures and inhospitable environment.

Concrete measures in this direction must be enforced by the government. Citizens should be given proper guidance. Measures to enhance awareness should be designed.

It is pathetic that America, the world’s most developed country has the ‘smallest fund of practical nutritional knowledge’ (Obesity in America).

To illustrate this point, Dr. Dean Ornish. M.D- Cardiologist said in an interview, “I’d love to be able to tell people that bacon and eggs are health food, but they are not.” “An easier way a fewer calorie is not just to change the amount of food but the type of food, because fat has 9 calories per gram, whereas protein and carbohydrates have only 4. So when you eat less fat, you eat fewer calories without having to eat less food.” (Interview Dean Ornish, M. D, 2004).

Dr. Ornish’s book Eat More, Weigh Less is based on this concept.

His method has been scientifically proven because it is based on abundance rather than on deprivation.

“You can eat when you’re hungry, you can eat until you’re full, and you still lose weight and keep it off…..” (Ornish).

Dr.Ornish further claims that his diet has been proven to stop or reduce heart disease and has been backed up by scientific studies. His claim and findings cannot be written off as our ancestors led a healthy life as they fed on food coming directly from the land. Obesity wasn’t even a word.

With modern technology, change in American diet and lifestyle, eating fast food, microwave dinners, and a diet of packaged, processed, and refined foods, the American finds himself digging his own grave. People with determination and a will to survive have succeeded in being healthy again. Alas! The number of such people is only a handful. Inevitably, processed food, fast foods, meat products, high sugar, and high sodium food have to be substituted by whole grains, vegetables, fruits, and legumes.

To substantiate the above statement, Nathan Sorensen, a leading dietician has outlined 10 important tips for a healthy eating habit.

• Eat breakfast daily.
• Plan your daily meals.
• Pack a fruit snack for the commute.
• Choose the smaller portion food entrée’s, if you eat out for lunch.
• Eat a snack when you get home; tortillas with salsa.
• Before grocery shopping, write a shopping list.
• Plan and prepare fish and vegetable meals weekly.
• Choose not to add fat to prepared foods.
• Eat dinner every night before 7.30P.M.
• Have a snack an hour or so before food. (Sorensen, 2008).

There have been innumerable articles, journals, and books written on this concern. Medical science has advanced to such an extent that it can provide a remedy to almost all ailments. Health is probably the only field wherein the individual has to equip himself before approaching his specialist on his predicament. The most important factor seems to be willpower and self- control. Yet another fact is a change in his lifestyle. The doctor is only a medium through which the individual can find a solution to his ailment, but the ultimate cure lies in the hands of the patient.

A nation can be adjudged the best by the quality of its products, its approach on the socio-economic and political fronts, individual expertise, and above all health. America stands ahead of all the nations in the world in all the above respects except, general health. This problem has assumed a gigantic proportion which requires total co-operation to the reduction of its size. By total co-operation, I mean the individual, the market, the government, and medical science sitting together to arrive at an amicable solution.

Americas Obesity Crisis . Time Online addition. 2004. Web.

Obesity . Wikipedia. 2008. Web.

Obesity Trends. ObesityinAmerica.org. 1991-2003. Web.

Obesity in America . Down to Earth. Natural Foods .2008. Web.

Ornish, Dean M. D.Interview Frontline. 2004. Web.

Sorensen, Nathan. Obesity in America. Food & Nutrition . 2008. Web.

To show the depth of the gravity of the situation, a survey was conducted and the results obtained was quite alarming. Nearly, 65% of adults in America are prone to obesity due to circumstances of the modern man’s life.

The percent obese graph listed below supports the view.

Age group 1991 1995 1998 2000 2001

18-29 7.1 10.1 12.1 13.5 14

30-39 11.3 14.4 16.9 20.2 20.5

40-49 15.8 17.9 21.2 22.9 24.7

50-59 16.1 21.6 23.8 25.6 26.1

60-69 14.7 19.4 21.3 22.9 25.3

>.70 11.4 12.1 14.6 15.5 17.1

An alarming upward trend is seen. (Obesity Trends, 1991-2003).

The US has the highest rate of obesity in the developed world. In 2004, the CDC reported that 66.3% of the adults in the US are overweight or obese. True but unbelievable, a stressful mentally and insufficient sleep could also result in obesity. Genetic reasons seem to be silent killers in this direction.

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IvyPanda. (2024, March 1). Obesity as a Worldwide Problem and Its Solution. https://ivypanda.com/essays/obesity-as-a-worldwide-problem-and-its-solution/

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IvyPanda . 2024. "Obesity as a Worldwide Problem and Its Solution." March 1, 2024. https://ivypanda.com/essays/obesity-as-a-worldwide-problem-and-its-solution/.

1. IvyPanda . "Obesity as a Worldwide Problem and Its Solution." March 1, 2024. https://ivypanda.com/essays/obesity-as-a-worldwide-problem-and-its-solution/.

Bibliography

IvyPanda . "Obesity as a Worldwide Problem and Its Solution." March 1, 2024. https://ivypanda.com/essays/obesity-as-a-worldwide-problem-and-its-solution/.

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• Published: 27 April 2024

Obesity-induced blood-brain barrier dysfunction: phenotypes and mechanisms

• Ziying Feng 1 , 2 ,
• Cheng Fang 1 ,
• Yinzhong Ma 1 , 3 &
• Junlei Chang 1 , 2 , 3  

Journal of Neuroinflammation volume  21 , Article number:  110 ( 2024 ) Cite this article

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Obesity, a burgeoning global health issue, is increasingly recognized for its detrimental effects on the central nervous system, particularly concerning the integrity of the blood-brain barrier (BBB). This manuscript delves into the intricate relationship between obesity and BBB dysfunction, elucidating the underlying phenotypes and molecular mechanisms. We commence with an overview of the BBB’s critical role in maintaining cerebral homeostasis and the pathological alterations induced by obesity. By employing a comprehensive literature review, we examine the structural and functional modifications of the BBB in the context of obesity, including increased permeability, altered transport mechanisms, and inflammatory responses. The manuscript highlights how obesity-induced systemic inflammation and metabolic dysregulation contribute to BBB disruption, thereby predisposing individuals to various neurological disorders. We further explore the potential pathways, such as oxidative stress and endothelial cell dysfunction, that mediate these changes. Our discussion culminates in the summary of current findings and the identification of knowledge gaps, paving the way for future research directions. This review underscores the significance of understanding BBB dysfunction in obesity, not only for its implications in neurodegenerative diseases but also for developing targeted therapeutic strategies to mitigate these effects.

Introduction

Obesity, characterized by excessive fat accumulation, represents a burgeoning health issue of global populations. The World Health Organization reports an alarming rise in obesity rates worldwide, with an estimated 2.5 billion adults being overweight (body mass index, BMI > 25), of which approximately 890 million are obese (BMI > 30) as of 2022 [ 1 ]. This pervasive phenomenon profoundly impacts human health, inciting a multitude of disorders including cardiovascular disease, stroke, diabetes, and certain types of cancer.

Of particular interest, however, is the intricate relationship between obesity and neurological disorders, a link that has increasingly captivated scientific attention. Alzheimer’s disease [ 2 , 3 , 4 ] and stroke [ 5 , 6 , 7 ], for instance, are two representative neurological disorders that have been recurrently associated with obesity. Recent evidence points to obesity as a critical risk factor for mitochondrial dysfunction, as astrocytic fatty acid oxidation (FAO) and oxidative phosphorylation (OxPhos) are involved in these lipid-involving neurodegenerative disorders, implicating obesity’s role in influencing the disease onset and progression [ 8 , 9 ]. This escalating prevalence of obesity and its potential implications for neurological disorders presents a grave concern for global health. It necessitates a comprehensive understanding of obesity’s detrimental consequences towards the central nervous system (CNS), specifically its effects on the cerebral vascular system.

A critical component of the cerebrovascular system is the blood-brain barrier (BBB), a critical function of brain blood microvessels that maintains CNS homeostasis. The BBB strictly regulates the exchange of substances between the blood and the brain. This dynamic barrier ensures the stability of brain microenvironment, protects against neurotoxins, and facilitates proper neuronal function [ 10 , 11 ]. However, in pathological states such as obesity, this pivotal barrier can be compromised, leading to various neurological disorders. Understanding the intricate relationship between obesity and BBB dysfunction therefore becomes a matter of paramount importance.

We aim to delve into the complexities of this relationship, exploring the phenotypes and underlying mechanisms of BBB dysfunction in obesity. Through a comprehensive examination of the current literature, we provide an in-depth analysis of the potential changes in BBB structure and function induced by obesity. Additionally, we elucidate the mechanistic pathways that may be implicated in BBB dysfunction in obesity. This review ultimately seeks to underscore the significance of understanding BBB dysfunction in obesity and its implications for neurological health, with the goal of guiding future research and clinical practice.

Blood-brain barrier: cellular and molecular components

The blood-brain barrier (BBB) is a sophisticated and highly specialized biological construct, known for its selective permeability and protective role within the CNS. It owes its unique functionality to its intricately assembled cellular and molecular components, which work together to maintain CNS homeostasis. The structural and functional foundation of the BBB is the neurovascular unit (NVU) [ 12 ], a complex ensemble encompassing brain endothelial cells (BECs), pericytes, astrocytes, extracellular matrix (ECM), microglia, and neurons (Fig.  1 ).

BBB integrated within the NVU . This diagram depicts the structural components of the blood-brain barrier (BBB) within the neurovascular unit (NVU), illustrating the tight junctions of endothelial cells, the supportive pericytes, and the encircling astrocytic end-feet. It highlights the BBB’s integral structural role in the NVU, which is essential for maintaining cerebral integrity and function

Endothelial cells

As the primary component of the BBB, brain endothelial cells (BECs), line the interior surfaces of the brain’s capillaries. These cells are distinctive in their unique morphology and possess attributes that separate them from peripheral ECs [ 13 , 14 , 15 ]. BECs are closely interconnected through tight junctions (TJs), which restrict the paracellular pathway and control the ionic balance across the barrier. This feature is instrumental in preventing the free passage of substances from the blood into the brain. BECs also exhibit limited pinocytic activity and lack fenestrations, thereby further restricting transcellular transport. In order to provide brain with abundant nutrients and a healthy environment, specific transporters which allows for the selective passage of molecules are expressed in BECs. Through analyzing single-cell RNA-sequencing data of mouse ECs from different organs provided by the Tabula Muris consortium, Paik et al. found that BECs possess not only its own unique transcriptomic identities, but also the most specialized differentially expressed genes (DEGs) profiles that expressed primarily solute carrier transporters [ 16 ]. For instance, glucose transporter protein-1(Glut-1) is responsible for transporting glucose, which being a crucial energy fuel, from blood to the brain [ 17 ]. On the other hand, P-glycoprotein (P-gp) acts as an efflux pump that removes harmful substances out of the brain to keep a safe environment [ 18 ].

Worth noticed, BECs can also transport molecules through low rates of transcytosis, a process that plays a vital role in endothelial transport [ 19 , 20 ]. Transcytosis allows for selective or non-selective passage of molecules across the endothelial cells. In BECs, transcytosis can be divided into receptor-mediated (selective) transcytosis, which includes the transport of transferrin and insulin, and bulk-phase or fluid-phase (non-selective) transcytosis, typically exemplified by the transport of albumin [ 21 ]. Notably, while native albumin crosses the BBB via non-selective bulk-phase transcytosis, cationic albumin is transported more efficiently as it engages in adsorptive transcytosis, highlighting the distinct pathways for different forms of albumin. A key regulator in this process is Major Facilitator Superfamily Domain Containing 2 A (Mfsd2a), which specifically inhibits bulk-phase transcytosis in BECs [ 22 ]. Mfsd2a modifies the lipid composition of the cell membrane, thereby limiting the formation of caveolae vesicles and reducing caveolae-mediated transcytosis. This action helps maintain the selective permeability and overall integrity of the BBB. Contrary to inhibiting all forms of transcytosis, Mfsd2a’s role is particularly pivotal in restraining non-selective transcytosis or bulk-phase transcytosis. Research indicates that overexpression of Mfsd2a in CNS endothelial cells leads to a decreased number of transcytotic vesicles, which in turn reduces hematoma levels and alleviates BBB injury in mouse models of intracerebral hemorrhage (ICH) [ 23 ]. This highlights the potential therapeutic value of Mfsd2a in mitigating BBB disruption by specifically targeting non-selective transcytosis mechanisms post-injury.

In comparison to endothelial cells found elsewhere in the body, brain endothelial cells (BECs) demonstrate a unique profile of leukocyte adhesion molecule (LAM) expression. This profile contributes to the CNS’s immune privilege by limiting the extravasation of leukocytes under normal conditions. While LAMs are integral to leukocyte adhesion and migration — key steps in the immune response — their regulated expression in BECs ensures a controlled interaction with leukocytes, thereby maintaining CNS homeostasis [ 24 ]. Contrary to the constant expression in peripheral tissues, the presence and activity of LAMs in the BBB vary contextually. Notably, BECs typically lack selectins in their Weibel-Palade bodies, which reduces their ability for rapid leukocyte recruitment compared to peripheral endothelial cells. This does not equate to a complete suppression of immune response but represents a finely tuned regulation ensuring selective leukocyte passage without compromising BBB integrity [ 25 ]. During certain pathological conditions, leukocytes such as neutrophils and T cells may interact with the BBB in ways that can affect its permeability, through the release of cytokines, reactive oxygen species, and other mediators. However, these interactions do not universally result in BBB disruption and can occur in the absence of significant leakage, depending on the specific disease context and the nature of leukocyte engagement. In the context of neuroinflammatory diseases, such as multiple sclerosis (MS), alterations in the expression and functionality of LAMs have been observed. These changes can facilitate increased adhesion of leukocytes to BECs, potentially leading to BBB disruption under these pathological states [ 26 ]. However, this process reflects a departure from the normative regulatory mechanisms in place under healthy conditions and underscores the complex role of LAMs in both maintaining CNS immunity and contributing to neuroinflammation when dysregulated.

Pericytes is a kind of multi-functional cells embedded within the walls of capillaries throughout the body, including the brain, and play a crucial role in maintaining the integrity of the BBB. They were first identified in the 1870s, and more recently, numerous vascular functions of pericytes have been identified. These include regulation of cerebral blood flow, maintenance of the BBB integrity, and control of vascular development and angiogenesis [ 27 , 28 , 29 ]. In addition to these roles, pericytes have been found to play an active role during neuroinflammation in the adult brain [ 28 , 30 , 31 ]. They can respond differentially, depending on the degree of inflammation, by secreting a set of neurotrophic factors to promote cell survival and regeneration, or by potentiating inflammation through the release of inflammatory mediators (e.g., cytokines and chemokines), and the overexpression of pattern recognition receptors [ 32 ]. In neuroinflammatory conditions like multiple sclerosis, pericytes undergo morphological changes, elongating their processes within inflamed perivascular cuffs [ 33 ]. Exposure to cytokines and extracellular matrix proteins like chondroitin sulfate proteoglycans enhances pericyte secretion of chemokines and promotes macrophage migration [ 33 ]. This implicates pericytes in propagating neuroinflammation through immune cell recruitment. However, pericytes also have neuroprotective capacities dependent on the degree of inflammation [ 34 ]. Through release of neurotrophic factors like BDNF, pericytes can promote neuronal survival and regeneration [ 35 ]. Their expression of cell adhesion molecules likewise facilitates interactions with endothelial cells and astrocytes to maintain cerebrovascular stability [ 36 ]. The dual functionality of pericytes is highlighted by their differential secretome profiles in response to IL-1β [ 37 ]. While pericytes secrete certain pro-inflammatory genes like CCL2 [ 38 ], they also show expression of vascular-stabilized mediators like TIMP3 [ 34 , 39 ]. This nuanced, context-dependent pericyte reactivity fine-tunes neuroinflammatory responses.

Pericyte dysfunction is increasingly recognized as a contributor to the progression of vascular diseases such as stroke and neurodegenerative diseases [ 40 , 41 ]. The therapeutic potential of pericytes to repair cerebral blood vessels and promote angiogenesis due to their ability to possess stem cell-like properties has recently been brought to light. In the context of cerebral blood vessels repair, pericytes can migrate to the site of injury and differentiate into cells that are needed for repair [ 42 , 43 ]. As for promoting angiogenesis, pericytes play a vital role in the formation of new blood vessels from pre-existing ones, a process known as angiogenesis [ 44 ]. They stabilize the newly formed endothelial tubes, modulate blood flow and vascular permeability, and regulate endothelial proliferation, differentiation, migration and survival. However, research has shown that pericytes and endothelial cells have overlapping but distinct secretome profiles in response to IL-1β [ 45 ]. This indicates that these two cell types may respond differently to inflammatory stimuli, which could have implications for understanding how inflammation affects the cerebrovasculature.

In conclusion, pericytes play a critical role in maintaining BBB integrity by controlling various processes. Understanding these mechanisms could provide valuable insights into BBB function and CNS immunity. Future research directions could include exploring the role of other proteins involved in these processes, further investigating the function of pericytes in disease states, and studying how changes in pericyte function could impact BBB integrity and CNS health.

Astrocytes, another critical component of the NVU, also play a crucial role in BBB maintenance. Their end-foot processes enwrap the brain capillaries and provide physical support to the BBB. Through their extensive contact with endothelial cells, astrocytes are vital in the formation and maintenance of the BBB. More specifically, astrocytes can secrete Sonic hedgehog (Shh), thereby stimulating the expression of TJs proteins and junctional adhesion molecule-A (JAM-A) while promoting immune quiescence of BBB by decreasing the expression of chemokines and LAMs [ 46 ]. The Hedgehog (Hh) pathway is involved in embryonic morphogenesis, neuronal guidance, and angiogenesis [ 47 ]. In adult tissues, it participates in vascular proliferation, differentiation, and tissue repair. The Hh pathway provides a barrier-promoting effect and an endogenous anti-inflammatory balance to CNS-directed immune attacks [ 48 ]. In terms of cerebrovascular accidents, astrocytes have been found to play a crucial role in maintaining blood-brain barrier function [ 49 ]. They support neurons and other glia, and react to changes in both the local and external environment. Beyond these homeostatic functions, astrocytes can respond to several stimuli and subsequently display profound genetic, morphological, and functional changes in a process termed reactive astrogliosis.

In addition to their role in maintaining BBB integrity, astrocytes also play a crucial role in controlling water homeostasis in the brain. Aquaporins (AQPs) are transmembrane proteins responsible for fast water movement across cell membranes, including those of astrocytes [ 50 ]. Various subtypes of AQPs (AQP1, AQP3, AQP4, AQP5, AQP8 and AQP9) have been reported to be expressed in astrocytes. The expressions and subcellular localizations of AQPs in astrocytes are highly correlated with both their physiological and pathophysiological functions [ 51 , 52 ].

Basement membrane

The basement membrane (BM) was secreted and maintained by BECs, pericytes and astrocytes. The BM is composed of various proteins, including Laminins, Collagen-IV, Perlecan, and Fibronectin [ 53 , 54 ]. These components interact with each other and with other cells at the BBB. For example, Laminins provide structural support to the BBB and are involved in processes such as cell adhesion, differentiation, migration, and apoptosis, while Collagen-IV provides mechanical strength to the BBB and contributes to its stability [ 53 , 54 ]. Any alterations in these components can lead to BBB dysfunction, which is associated with various neurological disorders. For instance, in conditions such as stroke, the BBB undergoes significant changes, including alterations in the expression of integrins and degradation of surrounding ECM, which indirectly affect the vascular barrier function [ 55 ]. In an animal model of autoimmunity, considerable information has been revealed about the function of different BMs in maintaining BBB integrity and causing neuroinflammation [ 56 , 57 , 58 ].

ECM receptors, such as integrins and dystroglycan, are also expressed at the brain microvasculature and mediate the connections between cellular and matrix components in physiology and disease [ 59 , 60 , 61 ]. These proteins and receptors elicit diverse molecular signals that allow cell adaptation to environmental changes and regulate growth and cell motility [ 62 ].

Microglia and neurons

Finally, microglia and neurons, while not directly forming the BBB, significantly contribute to its function and maintenance. Microglia, the resident immune cells of the brain, play a crucial role in maintaining the integrity of the BBB. Following ischemic stroke, microglia interact with endothelial cells in a paracrine manner to promote angiogenesis and barrier repair [ 63 ]. However, this reparative crosstalk is impeded in aging, implicating declined microglial function in age-related BBB disruption [ 64 ]. Accordingly, experimental depletion of microglia exacerbates injury and edema in aged mice subjected to ischemic stroke, further confirming microglia’s protective influence [ 65 ]. Beyond strokes, microglia also maintain BBB stability in neuroinflammatory conditions by modulating astrocyte reactivity and phagocytosing synapses [ 66 ]. In a model of multiple sclerosis, microglia limited astrocyte activation and protected against BBB leakage, stressing their homeostatic role [ 67 ]. During reactive gliosis induced by stroke, microglia and macrophages preferentially eliminated excitatory synapses while astrocytes cleared inhibitory synapses, preventing excessive imbalance of excitatory/inhibitory tone [ 67 ].These findings underscore diverse mechanisms whereby microglia maintain cerebrovascular equilibrium, ranging from paracrine support of angiogenesis to controlled synapse engulfment. Their protective influence likely declines with aging, permitting BBB hyperpermeability. Boosting microglial function represents a promising strategy to strengthen BBB integrity in neurological disorders.

Neurons also play a significant role in BBB’s function and maintenance. Neurons communicate with other components of the neurovascular unit (NVU), such as endothelial cells, pericytes, and astrocytes, to regulate BBB properties. This communication is also critical for maintaining the CNS homeostasis and for responding to changes in neural activity. In the early postnatal mouse barrel cortex, it was demonstrated that manipulations of sensory inputs resulted in vascular structural changes [ 68 ]. Specifically, this study showed that local sensory-related neural activity promoted the formation of cerebrovascular networks.

Neurovascular coupling refers to the relationship between local neural activity and subsequent changes in cerebral blood flow (CBF) [ 69 ]. The magnitude and spatial location of blood flow changes are tightly linked to changes in neural activity through a complex sequence of coordinated events involving neurons, glia, and vascular cells. This mechanism is crucial as it matches the high energy demand of the brain with a supply of energy substrates from the blood. Evoked the neural activity by high-intensity visual stimulation could drive macroscopic cerebrospinal fluid (CSF) flow in the human brain [ 70 ]. The timing and amplitude of CSF flow were matched to the visually evoked hemodynamic responses, suggesting neural activity can modulate CSF flow via neurovascular coupling.

In addition to their role in neurovascular coupling, neurons also contribute to BBB function through some transporters. It was found that neuronal activity regulates BBB efflux transporter expression and function [ 71 ], which is critical for excluding many small lipophilic molecules from the brain parenchyma. These findings suggest that sensory-related neural activity can influence both vascular structure and BBB function, which could have significant implications for understanding neuro-vascular interaction. An understanding of these intricate structures and their functions is pivotal in comprehending how pathological states, such as obesity, could affect the BBB and ultimately lead to neurological disorders.

Obesity-induced BBB leakage: phenotypes and mechanisms

The impact of obesity on BBB integrity has been an area of increasing scientific scrutiny, given the relationship between obesity and various neurological disorders. The disruption of BBB integrity or non-specific leakage of the BBB, as it is commonly referred to, is a recurrent phenotype observed in obesity, especially in the context of high-fat diet (HFD) intake with a wide duration from 8 to 36 w [ 72 , 73 , 74 , 75 ]. This section seeks to elucidate the molecular mechanisms and phenotypic changes underlying obesity-induced BBB leakage and associated BBB markers of this pathological state.

Changes in tight junctions

A key factor implicated in obesity-induced BBB leakage is the dysregulation of tight junction proteins (TJs). TJs, as earlier stated, are critical in maintaining the restrictive properties of the BBB. However, obesity, particularly under conditions of HFD, can alter the expression and function of these proteins. For instance, Ouyang et al. observed alterations in the expression levels of ZO-1 in microvessels from obese mice modeling by 8 weeks (w) of HFD [ 76 ]. In line with this observation, HFD significantly decreased the protein levels of ZO-1, Claudin-5 and Occludin along with the leakage of brain microvessles after 8 weeks (w) of HFD [ 77 ]. In adult rats, 90 days of high-energy diet (high in saturated fat and glucose) consumption decreased mRNA expression of TJs, particularly Claudin-5 and − 12, in the choroid plexus and the BBB. Consequently, an increased blood-to-brain permeability of sodium fluorescein was observed in the hippocampus [ 78 ]. This underscores the potential for obesity-induced modifications to BBB structure and function.

The adenosine receptor 2a (Adora2a) is increasingly recognized for its significant role in the modulation of neurovascular and neuroinflammatory responses. Activation of Adora2a receptors has been linked to heightened inflammatory responses, contributing to the disruption of the blood-brain barrier (BBB) and subsequent neuronal damage, conditions often exacerbated by obesity and metabolic syndrome. In a rodent model of diet-induced insulin resistance by 16 w of HFD, it was found that chronic activation of Adora2a eroded TJs between BECs, as evidenced by diminished Occludin and Claudin-5 in hippocampal lysates. Considering the detrimental effects associated with Adora2a activation on BBB integrity, antagonism of this receptor presents a promising therapeutic strategy. By inhibiting Adora2a, it is possible to mitigate the receptor-mediated exacerbation of inflammatory processes within the CNS, thereby preserving BBB function and reducing neuroinflammatory sequelae. This premise is supported by several studies demonstrating that Adora2a antagonists can effectively reduce BBB permeability and alleviate inflammatory damage in various neuroinflammatory and neurovascular disorders [ 79 , 80 , 81 ].

In addition, it is noteworthy that obesity not only affects one’s own BBB function, but also has an impact on its offspring. A recent study showed that maternal obesity during pregnancy could impaired BBB formation of the fetal, leading to changes in TJ components of the arcuate nucleus region in offspring’s brain, thereby significantly increasing BBB permeability [ 82 ]. This dysregulation of TJs compromises the integrity of the BBB, increasing its permeability and enabling the passage of potentially harmful substances from the blood into the CNS. Interestingly, recent studies have also linked prolonged HFD intake for 32 w to anxiety-like and depression-like behaviors in mice [ 83 ]. It was found that 24 weeks of HFD consumption induced neurobehavioral deterioration, including increased anxiety-like and depression-like behavior. These behavioral changes were associated with impaired gut microbiota homeostasis and inflammation. Long term HFD may induce certain behavioral phenotypes related to neurological disorders through the gut-brain axis [ 83 ]. In line with this, treatment with the anti-inflammatory molecule palmitoylethanolamide was found to reduce anxiety-like behavior in obese mice modeling by 19 w of HFD, along with dampening systemic and central inflammation [ 84 ]. Taken together, these studies suggest prolonged HFD may not only directly disrupt TJs and BBB integrity through inflammatory and other mechanisms, but also trigger neurobehavioral changes that could secondarily impact BBB function.

Changes in fenestration

As mentioned above, BECs are characterized by a lack of fenestrations, a characteristic that contributes to the high selectivity and restrictive nature of the BBB. Stan et al. identified PV-1 (also known as PLVAP, plasmalemma vesicle-associated protein; or MEGA-32 antigen) as a component of fenestral diaphragms in endothelial cells [ 85 ]. As PV-1 comprises these structures, its regulation could influence fenestration numbers. While PLVAP expressed on fenestrated endothelia and associated with the formation of diaphragms in vesicular structures, it does not serve as a marker for fenestrations within the BBB context. Instead, increases in PLVAP expression may reflect alterations in the molecular composition associated with transcellular pathways rather than the formation of true fenestrae. In a single-cell profiling study, analysis of BECs revealed that among eight major clusters, fenestrated BECs in areas such as the choroid plexus showed the most unique obesity-induced DEGs, where fenestrated endothelia are typical, rather than suggesting the emergence of fenestrations within the BBB due to obesity modeling by 12 w of HFD [ 86 ]. In line with this, Previous study have demonstrated that HFD intake can lead to an increase in endothelial fenestration in the BBB, such as the observed changes in the offspring of gestational obesity in mice [ 82 ]. Worth noticed, these findings, particularly those related to increased permeability in regions like the arcuate nucleus, may reflect localized alterations in BBB properties rather than systemic induction of fenestrations akin to those in inherently fenestrated structures like the choroid plexus.

Therefore, while the effects of HFD on endothelial cell biology are undeniable, the notion that these effects lead to the formation of fenestrations within the typical BBB structure remains debatable. This perspective allows for the possibility that PLVAP-regulated alterations may occur regionally within specific areas of the brain under certain conditions, rather than implying a global change across the entire barrier. The DEGs identified in obesity models, particularly those affecting endothelial cells of the BBB, should be interpreted with an understanding that obesity-induced stress may lead to changes in molecular signaling and barrier properties without necessitating the creation of actual fenestral openings.

Changes in matrix metalloproteinases

Matrix metalloproteinases (MMPs) are a family of endopeptidases that function to degrade and remodel the extracellular matrix (ECM). MMPs are secreted by various cell types including epithelial cells, fibroblasts, and inflammatory cells, playing important roles in physiological processes as well as disease states characterized by tissue damage and inflammation. However, excessive MMPs can lead to pathological ECM degradation and impairment of tissue structure and function, as in the case of blood-brain barrier (BBB) disruption by MMP-2 and MMP-9 [ 87 , 88 , 89 ]. Obesity has been linked to increased expression and activity of certain MMPs, which can impair BBB integrity. For example, plasma MMP-9 levels were found to be elevated in obese subjects and decreased with anti-diabetic treatment [ 90 , 91 ]. Cotemporally, lipocalin-2 was also increased in adipose tissue of obese individuals and correlated with MMP-2 and MMP-9 activity [ 92 ]. MMP-8 levels were similarly increased in obesity and associated with insulin resistance [ 93 ]. Additional studies have assessed levels of MMPs like MMP-2 and MMP-9 along with their inhibitors TIMPs in obese children [ 94 ]. Together, these findings suggest obesity creates a pro-inflammatory state characterized by upregulation of MMPs like MMP-8 and MMP-9, potentially driven by increases in mediators like lipocalin-2. By degrading ECM proteins, these MMPs can impair BBB structural integrity. A general description of obesity-induced BBB leakage was shown in Fig.  2 .

Mechanisms of Obesity-Induced BBB Leakage. Illustration of the complex alterations in the BBB induced by obesity, highlighting the loosening of endothelial cell junctions, increased permeability, and the unusual occurrence of fenestrations. These structural changes are further exacerbated by the activity of MMPs, which degrade extracellular matrix components, facilitating the infiltration of peripheral immune cells, such as neutrophils. This cascade of events underscores the multifaceted and interconnected impact of obesity on BBB integrity and the resulting immune response within the cerebral vasculature

Obesity-induced BBB transport dysfunction: phenotypes and mechanisms

In addition to disrupting the BBB integrity, obesity is associated with alterations in the BBB’s transport functions. These changes not only affect the nutrient supply to the brain but can also influence the entry and clearance of toxins, signaling molecules, and therapeutics. The transport across the BBB is highly regulated, with specific receptors and transporters expressed in BECs mediating the process. However, obesity can induce significant changes in these receptors and transporters, leading to BBB transport dysfunction.

Glucose transport-1 (Glut-1)

One of the key alterations in BBB transport function under obesity conditions is the dysregulation of glucose transport. The primary transporter responsible for glucose transport across the BBB is the glucose transporter 1 (Glut-1), which ensures the supply of glucose from the blood to the brain. However, in the state of obesity, particularly in HFD-induced obesity, the expression and function of Glut-1 have been found to be altered. Specifically, studies in mouse models have demonstrated that acute high-fat feeding for 2–3 days suppressed Glut-1 expression and glucose uptake in the brain [ 95 , 96 ]. Similarly, the mouse insulin resistance model showed that when 2 weeks of HFD significantly downregulated the expression of Glut-1 in the brain, 10 weeks of HFD normalized the expression of Glut-1, suggesting the duration of insulin resistance may influenced the regulation of Glut-1 [ 97 ]. In humans, genetic factors were found to impact Glut-1 levels, which in turn modulates cognitive effects of high-fat intake [ 98 ].

Interestingly, upon more prolonged high-fat feeding for 10 weeks, Glut-1 expression was restored, which was related to the initiation of compensatory mechanisms of vascular endothelial growth factor (VEGF), a key regulator of angiogenesis and vascular function [ 95 ]. Recent studies have illuminated the role of VEGF in respond to metabolic stresses and hypoxic conditions often prevalent in obesity. This response includes the potential to upregulate Glut-1 expression, ostensibly to compensate for altered metabolic demands and ensure sufficient glucose transport across the BBB. However, the interplay between VEGF and Glut-1 in the setting of obesity is multifaceted. While moderate increases in VEGF can be beneficial, aiding in the restoration of Glut-1 levels and maintaining cerebral glucose metabolism, chronic elevations—common in prolonged obesity—may lead to adverse effects [ 95 , 96 ]. Excessive VEGF can contribute to vascular abnormalities and exacerbate BBB disruption, complicating the metabolic landscape of the CNS. Therefore, understanding the dynamic between VEGF-induced Glut-1 modulation and obesity provides insight into the broader implications of metabolic syndrome on BBB health and brain metabolism. This section explores how the nuanced changes in VEGF and Glut-1 expression influenced by obesity underscore the complexity of maintaining BBB integrity and highlight the need for targeted therapeutic strategies to address these metabolic challenges.

Taken together, while short-term high-fat intake appears to impair Glut-1 function and glucose transport at the BBB, compensation may occur with prolonged obesity to normalize Glut-1 expression. However, the brain is the most energy-consuming organ, requiring constant high energy to maintain its function, thereby the temporary disruption in glucose delivery to the brain may be sufficient to impact neuronal health and cognition. Further research into the kinetics of Glut-1 regulation in response to high-fat feeding could delineate the timeframe of BBB transport deficits. This may provide insights into critical windows where impaired brain glucose uptake contributes to neurological disorders associated with obesity.

Alterations in insulin transport have also been observed in obesity, which can profoundly impact neuronal function. Insulin enters the brain via saturation transport and binds to insulin receptors (IR) on BECs, triggering receptor autophosphorylation and downstream signaling cascades involved in glucose uptake, metabolism, neuronal plasticity and survival [ 99 ]. However, studies in obese animal models and human subjects indicate that obesity and HFD feeding can impair insulin transport across the BBB. In preclinical studies using mouse and canine models, HFD feeding for 7 w reduced transport of intravenously injected insulin from the circulation into the brain parenchyma [ 100 , 101 ]. This reduction is associated with central insulin resistance, as evidenced by impaired insulin receptor signaling cascades in the brain from mice subjected to 4 w of HFD [ 102 ]. In human clinical studies, obese subjects were found to have lower cerebrospinal fluid (CSF) insulin levels and attenuated CSF insulin increases after systemic insulin infusion compared to healthy controls [ 103 ]. Together, these animal and human studies demonstrate that obesity disrupts brain endothelial insulin transport, reducing insulin delivery to the CNS. This transport dysfunction contributes to central insulin resistance, a phenomenon often linked with cognitive dysfunction and neurological disorders [ 104 ]. Consistence with this, brain insulin resistance has been recognized as an early characteristic of Alzheimer’s disease [ 105 ]. Elucidating the mechanisms by which high-fat feeding alters insulin receptor expression, trafficking and downstream signaling at the BBB will be critical for developing therapeutic strategies to overcome CNS insulin resistance.

In addition to insulin, the transport of the hormone leptin across the BBB is also altered in obesity. Leptin is also transported into the brain via a saturable transport system and binds to leptin receptors on neurons involved in regulating food intake and energy expenditure. However, multiple studies indicate HFD-induced obesity impairs leptin transport across the BBB. For instance, in obese individuals, the transport level of leptin to the brain is downregulated, as evidenced by a significantly lower ratio of the leptin cerebrospinal fluid (CSF)/serum compared to the healthy lean individuals [ 106 , 107 ]. In obese animal models including rodents subjected to 10 w of HFD and sheep subjected to 40 w of HFD, there is a significant decrease in the rate of leptin transport from blood to brain compared to lean controls [ 108 , 109 , 110 ]. Obesity can inhibit the transport of leptin across the BBB, making it impossible for the brain to receive the “satiety signal” emitted by leptin, leading to overeating and worsening of obesity, which may lead to a series of metabolic diseases. Of notice, with the development of obesity, obese mice modeling by 56 days of HFD respond to leptin for central administration (intracerebroventricularly) rather than peripheral administration (intraperitoneally or subcutaneously) [ 111 , 112 ]. This suggests that. the impairment in leptin transport does not appear to be due to altered leptin receptor expression at the BBB. Rather, transport may be inhibited due to saturation of the carrier system and interactions with other circulating factors, such as the high-level triglycerides [ 113 , 114 , 115 ]. Overall, these findings indicate obese states inhibit leptin’s ability to enter the CNS and bind neuronal targets, despite normal BBB leptin receptor levels. Overcoming the transport block could potentiate leptin’s effects on appetite and weight regulation.

P-glycoprotein (P-gp)

Obesity also affects the function of efflux transporters at the BBB, such as the P-glycoprotein (P-gp). P-gp is an ATP-dependent transporter that functions to pump foreign substances and metabolites out of the brain back into the bloodstream. This helps protect the brain from accumulation of potentially toxic compounds. P-gp is encoded by the ABCB1 gene. A human study found a negative correlation between BMI values and the expression levels of ABCB1 in the brain, suggesting P-gp levels are reduced in obesity [ 116 ]. While the mechanisms linking obesity to P-gp regulation require further elucidation, systemic inflammation appears to play a role. In obese pregnant mice, placental P-gp expression was decreased in tandem with increases in inflammatory cytokines like tumor necrosis factor-alpha (TNF-α), interleukin-1 beta (IL-1β), and interleukin-6 (IL-6) [ 117 ]. Changes in P-gp likely impair efflux of substrates from the brain back into circulation. Overall, although there is limited research on obesity and P-gp, current evidence indicates obesity can suppress P-gp expression and function at the BBB, at least in the obese human. This impairment in a key transporter for xenobiotic clearance may enable accumulation of toxins and drugs in the brain.

L-type amino acid transporter-1 (LAT1)

Amino acid transporters are also affected by obesity. The system L amino acid transporter 1 (LAT1) expressed at the BBB is responsible for transport of large neutral amino acids like leucine into the brain. LAT1 plays a key role in regulating mTORC1 signaling, which controls processes like protein synthesis and autophagy [ 118 ]. Recent studies have found that LAT1 function is altered in obesity models. Mice lacking neuronal LAT1 develop obesity phenotypes including increased adiposity [ 119 ]. LAT1 expression and amino acid uptake are reduced in the hypothalamus of obese, diabetic mice [ 120 ]. In humans, lower expression of the related transporter SLC7A10/ASC-1 in adipose tissue is associated with increased visceral fat, insulin resistance, and adipocyte hypertrophy [ 121 ]. Together, these findings indicate obesity impairs the function of multiple amino acid transporters at the BBB and periphery. This likely dysregulates mTORC1 signaling and other nutrient-sensing pathways, contributing to metabolic dysfunction. The alterations of transporters expressed in endothelial cells was summarized in Fig.  3 .

Obesity-Induced Alterations in BBB Transporters. This figure demonstrates the effects of obesity on BBB transporters: Glut-1 function is initially impaired by high-fat intake but may be normalized with prolonged obesity, despite potential impacts on neuronal health and cognition. Brain endothelial insulin transport is disrupted, contributing to central insulin resistance, and often associated with cognitive dysfunction and neurological disorders. Leptin transport impairment is linked to carrier system saturation, independent of leptin receptor expression changes. Obesity suppresses P-glycoprotein expression and function, potentially increasing brain accumulation of toxins and drugs. LAT1 expression and amino acid uptake are reduced in the hypothalamus of obese, diabetic mice, reflecting impaired amino acid transporter function at the BBB.

Evidence of BBB disruption in obesity and type 2 diabetes

Recent evidence has increasingly indicated that metabolic disorders such as obesity and Type 2 Diabetes (T2D) are closely linked to the disruption of the BBB. This section aims to elucidate the relationship between these conditions and BBB integrity, underpinned by recent scientific findings.

BBB Permeability in Type 2 Diabetes: Among the most compelling evidence in this domain is the study conducted by Starr and colleagues [ 122 ], which has demonstrated a significant increase in BBB permeability to gadolinium in patients with well-controlled T2D. This landmark study utilized advanced magnetic resonance imaging techniques to compare BBB integrity between diabetic patients and healthy individuals. The results indicated a pronounced increase in BBB permeability, notably in the basal ganglia region, suggesting a direct impact of T2D on neurovascular integrity. These findings are critical as they highlight the potential for well-controlled T2D to contribute to BBB dysfunction independently of other comorbidities often associated with metabolic syndrome.

The link between obesity and BBB disruption has been further substantiated by studies investigating the levels of specific BBB markers in obese individuals. A longitudinal perspective explores how factors related to adiposity in mid-life can have long-lasting effects on BBB integrity. The study highlights the enduring impact of obesity on neurovascular health, suggesting that the consequences of increased body weight extend far beyond the immediate metabolic disturbances commonly associated with obesity [ 123 ]. Another study focused on Adipsin, a complement system component known to be influenced by adiposity levels, and studied within the cerebrospinal fluid, providing insights into the biochemical pathways through which obesity might mediate changes in BBB integrity. This research suggests a direct link between metabolic health markers and the biochemical status of the BBB, illustrating the intricate connection between systemic metabolic health and neurovascular function [ 124 ]. These studies have shown elevated levels of certain markers, indicating compromised BBB integrity in the context of excessive body weight and associated metabolic derangements. The disruption is believed to be multifactorial, involving mechanisms such as increased systemic inflammation, altered lipid metabolism, and hypertension, all of which are prevalent in obesity and can adversely affect the endothelial cells constituting the BBB.

The mechanistic pathways through which obesity and T2D exacerbate BBB disruption are complex and multifaceted. Inflammatory cytokines, often elevated in obesity and T2D, are known to compromise BBB integrity by altering tight junction protein expression and endothelial cell function. Additionally, the hyperglycemic environment in T2D can induce oxidative stress and microvascular complications, further impairing BBB function. These alterations not only have direct implications for neurovascular health but also predispose individuals to a range of neurological disorders. Takechi et al. [ 125 ] shows that BBB dysfunction precedes cognitive decline and neurodegeneration in a diabetic insulin-resistant mouse modeled by 24 w of high fat and fructose fed, which may imply a causal link. Although this study is more centered around diabetes, the intersection with obesity (through insulin resistance) makes it pertinent. The above findings emphasizing the need for comprehensive management of these metabolic conditions to maintain BBB integrity and overall brain health.

In summary, the accumulating evidence underscores a significant association between obesity, T2D, and BBB disruption. This relationship highlights the importance of managing these metabolic disorders not only for cardiovascular health but also for maintaining the integrity of the neurovascular unit. As research in this field continues to evolve, understanding the specific pathways and impacts will be crucial for developing targeted interventions aimed at preserving BBB integrity in the face of growing obesity and T2D prevalence.

Obesity-induced neuroinflammation: phenotypes and mechanisms

Neuroinflammation, characterized by the activation of resident brain cells (microglia and astrocytes) and infiltration of peripheral immune cells, has been widely recognized as a critical pathological feature of obesity. The increased BBB permeability induced by obesity, as discussed earlier, not only allows harmful substances to penetrate into the CNS but also paves the way for peripheral immune cells to infiltrate the brain. Once in the CNS, these immune cells can instigate an inflammatory response, contributing significantly to obesity-induced neuroinflammation.

Microglia, the primary immune cells of the CNS, show enhanced activation in obesity. Once activated, microglia release a plethora of pro-inflammatory factors, including cytokines like TNF-α, IL-1β, and IL-6, thereby promoting a pro-inflammatory environment within the CNS [ 84 , 126 , 127 , 128 ]. In the research employed bone marrow chimerism mouse subjected to 15 or 30 w of HFD, it was also found that the aggregated inflammatory monocytes/macrophages located in the parenchyma and expressed the microglial marker Iba1 [ 129 ]. Notably, while microglia often exhibit a pro-inflammatory phenotype in the early stages of HFD-induced obesity, their activation state appears to change over time with prolonged exposure. As the study by Baufeld et al. [ 130 ] demonstrated, the initial microglial reaction in the hypothalamus of mice with 3 days of HFD was not accompanied by sustained increased pro-inflammatory cytokines with prolonged 20 w of HFD consumption. Rather, anti-inflammatory genes were upregulated while microglial sensing genes were downregulated [ 130 ]. This indicates that microglia may shift to a more anti-inflammatory or homeostatic phenotype after longer-term HFD consumption.

The regional heterogeneity of microglial responses is another important consideration. Microglia in the hypothalamic arcuate nucleus, for instance, displayed a markedly reaction to 8 weeks of HFD in a region-specific manner [ 130 ]. This underscores how microglia in different brain regions may uniquely adapted to their specific microenvironments and react differently to the metabolic challenges imposed by obesity. Furthermore, the plasticity and ability of microglia to respond to additional stimuli was preserved even after prolonged HFD feeding. When stimulated with LPS ex vivo after 8 weeks of HFD, hypothalamic microglia upregulated inflammatory genes comparable to microglia from control diet mice [ 130 ]. This indicates the microglia retain responsiveness despite adapting to the HFD conditions. Mechanically, Kim et al. [ 131 ] has been instrumental in highlighting the dynamic increase in uncoupling protein 2 ( Ucp2 ) mRNA expression in the hypothalamic microglia of mice following an 8 w-HFD regimen. This increase influences mitochondrial modifications that activate microglia, further contributing to hypothalamic inflammation and the overall susceptibility to obesity. In summary, emerging evidence indicates microglial phenotypes and functions are altered in a temporal and spatial manner by obesity and HFD consumption. While often displaying pro-inflammatory features acutely, microglia may adapt with anti-inflammatory or homeostatic responses over time. Their heterogeneous phenotypes across brain regions and retained ability to respond to stimuli highlight the complexity of microglial reactions in obesity.

Astrocytes, another critical cell type in the CNS, undergo reactive astrogliosis in obesity, characterized by changes in their morphology, proliferation, and function. Similar to microglia, activated astrocytes can also secrete pro-inflammatory cytokines, further exacerbating the neuroinflammatory response. Astrocytes in 16 w-HFD consumption displayed reactive astrogliosis, characterized by altered morphology and upregulation of intermediate filaments like glial fibrillary acidic protein (GFAP) [ 132 ]. This phenotypic shift was observable early during HFD feeding, even preceding substantial weight gain. Lin et al. [ 133 ] elucidates the upregulation of disease-associated astrocyte (DAA) and microglia markers in response to an 12 w-HFD that are similar to the pathogenesis of Alzheimer’s disease. providing a direct link between dietary habits, neuroinflammation, and neurodegeneration.

The functional profile of astrocytes was also altered by obesity-induced astrogliosis. Activated astrocytes upregulate expression of pro-inflammatory cytokines, including IL-6, IL-1β, and TNF-α in mice following an 11 w-HFD regimen [ 134 ]. This creates a self-perpetuating cycle, as increased cytokine levels can further stimulate astrogliosis. Additionally, aberrant release of gliotransmitters like glutamate from reactive astrocytes can also occur, potentially impacting neuronal excitability after a 16 w of HFD [ 126 ].

Multiple signaling pathways have been implicated in driving the astrogliotic transformation of astrocytes in obesity. As Thaler et al. demonstrated, astrocyte-specific inhibition of IKKβ/NF-κB signaling mitigated weight gain, glucose intolerance, and hypothalamic inflammation induced by 11 w of HFD consumption [ 134 ]. This suggests the IKKβ/NF-κB pathway is critical for obesity-related astrogliosis and its metabolic consequences. Calcineurin signaling has also been linked to astrocyte reactivity in response to HFD for 16 w [ 132 ]. Calcineurin inhibition attenuated gliosis in the arcuate nucleus, ventromedial hypothalamus, and dorsomedial hypothalamus of HFD mice. This implicates calcineurin/NFAT as another important mediator of astrocyte activation. In summary, the morphological and functional changes accompanying astrogliosis position astrocytes as key propagators of neuroinflammatory responses in obesity models induced by high-fat feeding. Delineating the intracellular signaling pathways driving these astrocyte alterations, such as IKKβ/NF-κB and calcineurin/NFAT, will contribute to uncover therapeutic targets for mitigating obesity-associated hypothalamic inflammation.

Monocytes/macrophages

Peripheral immune cells, particularly monocytes, have been reported to infiltrate the CNS in obesity. These monocytes can differentiate into macrophages, producing a variety of pro-inflammatory cytokines that exacerbate neuroinflammation. For instance, a bone marrow chimerism mouse model demonstrated that 15 or 30 w of HFD-induced obesity led to a 30% increase of immune cells in the CNS compared to controls [ 129 ]. Most of these cells exhibited a microglia/macrophage phenotype, being CD45 + CD11b + . The ratio of CD11b + CD45 hi to CD11b + CD45 lo cells was elevated, indicating an inflammatory state. In addition to the infiltration, HFD also promotes the differentiation of monocytes into macrophages. It was demonstrated that 14 w of HFD consumption induced the Ly6c high monocytes to differentiate into macrophages in the brain [ 135 ]. Another study showed that prolonged HFD consumption for 4 and 20 w led to expansion of the monocyte-derived macrophage pool in the hypothalamic arcuate nucleus, attributed to enhanced macrophage proliferation [ 136 ]. In mouse models of leptin receptor deficiency, breakdown of the BBB was found to enable macrophage infiltration into the brain of db/db mice [ 137 ]. Leptin resistance, glucose intolerance, and elevated cytokines like IL-1β and TNF-α accompanied the accumulation of macrophages. Notably, this study also suggested that IL-1β potentially play an important role in trafficking of peripheral monocytes into the brain. Overall, these studies indicate HFD-induced obesity facilitates the recruitment and proliferation of macrophages in the brain, propagating inflammation.

While the involvement of monocytes and macrophages in mediating neuroinflammatory responses under obese conditions is evident, it is imperative to scrutinize the methodologies employed in these studies for potential confounding factors. Specifically, investigations utilizing GFP bone marrow chimeras, such as those by Buckman et al. [ 129 ] and Baufeld et al. [ 130 ] mention above, provide critical insights into the trafficking of these immune cells in the context of obesity. However, the integral role of radiation treatment in these experimental designs warrants a careful evaluation of its impact on the observed outcomes. Radiation used to establish bone marrow chimeras, as a preparatory step for tracking immune cell migration, is known to independently alter BBB permeability and trigger pro-inflammatory responses, as detailed by Kierdorf et al. [ 138 ] This raises important considerations for interpreting studies on obesity-associated neuroinflammation: the increased permeability of the BBB and the augmented infiltration of monocytes/macrophages observed could be confounded by the radiation treatment itself, rather than being solely attributable to the effects of obesity.

Acknowledging these potential confounding effects is crucial for a comprehensive understanding of the dynamics between obesity and neurovascular integrity. Future research aimed at elucidating the specific roles of monocytes and macrophages in obesity-induced BBB disruption and brain inflammation should consider employing alternative methodologies that circumvent the need for radiation-induced bone marrow ablation. This approach will ensure a clearer delineation of the direct consequences of obesity on neuroimmune interactions and BBB integrity, free from the complicating effects of experimental interventions.

By carefully considering these methodological nuances, we can enhance our understanding of the complex interplay between obesity, BBB integrity, and the role of monocytes/macrophages in neuroinflammation, thereby paving the way for more targeted and effective therapeutic strategies.

Pro-inflammatory factors

Obesity-induced neuroinflammation is also marked by elevated expression levels of pro-inflammatory factors. In addition to TNF-α, IL-1β, and IL-6, other pro-inflammatory molecules such as inducible nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2) show increased expression in obesity. These molecules, produced by both infiltrating peripheral immune cells and activated resident brain cells, not only propagate inflammation but can also contribute to BBB disruption and neuronal damage. In human frontal cortex, it was reported that increased BMI has been found to cause iNOS-mediated inflammatory activity [ 139 ]. A recent finding demonstrated that iNOS promotes hypothalamic insulin resistance in obese rats. Aberrant nitrosative stress such as S-nitrosatiion (also referred to as S-nitrosylation) is closely associate with various neurological disorders such as AD and Parkinson’s Disease (PD) [ 140 , 141 ]. Inhibition of central iNOS ameliorated not only glucose metabolism, but also macrophage activation induced inflammation in hypothalamus of HFD-induced obesity mice [ 136 ]. In addition, 18 or 20 w of HFD consumption also can significantly enhance the expression of COX-2 in the hippocampus of the mice [ 142 , 143 ]. An increased activity of COX-2-PEG2 signaling pathway has been considered to play a key role in impairing hippocampal neuronal function and cognition [ 144 , 145 ].

Additionally, the aberrant activation of the inflammasome complexes, especially NOD-like receptor thermal protein domain associated protein 3 (NLRP3), plays a vital role in obesity-induced neuroinflammatory [ 146 ]. Within the CNS, microglia accumulate lipid droplets and activate NLRP3 inflammasomes under hyperglycemic conditions due to impaired lipophagy [ 147 ]. The microglial specific inflammatory amplifier TREM1 (triggering receptor expressed on myeloid cells), resulting in the buildup of microglial TREM1, was found to aggravates the HG-induced lipophagy damage and subsequently promoted HG-induced neuroinflammatory cascades via NLRP3 (NLR family pyrin domain containing 3) inflammasome. Pharmacological blockade of TREM1 with LP17 in db/db mice and HFD/STZ mice inhibited accumulation of lipid droplets and TREM1, reduced hippocampal neuronal inflammatory damage, and consequently improved cognitive functions [ 147 ].

Together, these diverse peripheral and central inflammatory pathways contribute to BBB disruption, neurotoxicity, and cognitive deficits associated with obesity. Targeting shared processes like nitrosative stress, which interacts with iNOS signaling, may simultaneously mitigate obesity-related neuroinflammation. The upregulation of pivotal inflammatory enzymes like iNOS and COX-2 highlights the multi-faceted nature of obesity-induced inflammation and the need for strategies that address key underlying pathways.

Mechanisms of Obesity-Induced Neuroinflammation . Enhanced microglial activation in obesity leads to increased release of pro-inflammatory cytokines (TNF-α, IL-1β, IL-6), contributing to a pro-inflammatory CNS environment. Concurrently, obesity triggers reactive astrogliosis in astrocytes characterized by morphological and functional changes, and secretion of pro-inflammatory cytokines. The infiltration of peripheral monocytes into the CNS, and differentiation into macrophages further exacerbates neuroinflammation through additional cytokine production. Elevated expression of pro-inflammatory factors such as iNOS and COX-2 in obesity are also depicted, highlighting their potential role in neuroinflammation, BBB disruption, and neuronal damage

Dietary influences on BBB integrity and obesity outcomes

The intricate relationship between obesity and inflammation underscores the multifaceted nature of BBB dysfunction. While the systemic inflammation associated with obesity undoubtedly impacts BBB integrity, it is imperative to address the direct and indirect effects of dietary patterns on neurovascular health. The link between diet, obesity, and BBB integrity provides a unique lens through which to understand the broader implications of nutritional habits on cerebral health and disease susceptibility. Freeman et al. [ 148 ] highlights the adverse effects of a 6 month consumption of high-fat/high-cholesterol (HFHC) diet on BBB function, demonstrating a reduction in BBB integrity markers and an increase in inflammatory responses within the hippocampus in middle-aged rats. This suggests that HFHC diets, beyond contributing to obesity, may directly compromise the BBB, thereby facilitating a neuroinflammatory state that could underpin cognitive decline. Similarly, Davidson et al. [ 149 ] reported on the effects of high-energy diets on hippocampal-dependent cognitive functions and BBB integrity. Their findings emphasized that diets high in saturated fats and sugars, hallmarks of the “Western” diet, not only contribute to obesity but also impair types of learning and memory dependent on the hippocampus. The unique aspect of this research is the differentiation between diet-induced obese and diet-resistant rats, highlighting how diet affects cognitive function and BBB integrity differently based on individual susceptibility to obesity. This is particularly concerning as it implies that dietary components can directly influence cognitive functions by altering hippocampal integrity and possibly disrupting the BBB. The dietary components and direct influences on BBB was detailed in Table  1 , which underscores the potential for dietary modifications as preventive or mitigative strategies against obesity-induced neurovascular alterations.

Emerging therapeutic strategies in tackling obesity-induced BBB dysfunction

In addressing the complexities of obesity-induced metabolic syndrome and its impact on the central nervous system, a spectrum of experimental therapies is currently under investigation, each targeting distinct pathological mechanisms. One promising approach involves the decrease of BBB permeability. Agents such as Palmitoylethanolamide, Topiramate, and Nicotine have demonstrated potential in modulating BBB dynamics, suggesting a pivotal role in mitigating obesity-related neurological sequelae in mice subjected to 10–36 w of HFD or 10 w of high saturated fatty acids diet consumption [ 72 , 73 , 84 ]. Among these, Palmitoylethanolamide has shown promise, not only in attenuating anxiety-like behavior but also in modulating neurotransmitter levels such as dopamine turnover and γ-aminobutyric acid (GABA) levels in the amygdala from mice subjected to 19 w of HFD consumption [ 84 ]. Additionally, it has been found to reduce systemic inflammation markers like TNF-α and IL-1β, attenuate hypothalamic injury, and decrease neuroinflammation and BBB permeability in the hippocampus. However, while its effects on BBB permeability are notable, further investigation is necessary to fully understand its long-term efficacy and safety profile, particularly in relation to chronic administration and potential systemic effects.

Topiramate, another therapeutic agent, has been demonstrated its capability to decrease BBB permeability in mice subjected to 13 and 36 w of HFD [ 72 ]. It achieves this through increasing the expression of tight junction proteins like ZO-1 and Claudin-12, which are crucial in maintaining BBB integrity. Topiramate also exhibits properties that inhibit oxidative stress, a common pathological feature in obesity-related neurological disorders. In this regard, agents like Dapsone and Resveratrol have garnered attention for their potential to protect tight junctions and reduce BBB disruption in mice following 8 w of HFD [ 74 , 77 ]. Dapsone, for instance, has been found to decrease brain microvascular leakage, which is often exacerbated in obesity. It does so by inhibiting the oxidation of low-density lipoproteins (LDL), a process that is detrimental to the BBB [ 77 ]. Additionally, Dapsone has shown efficacy in protecting tight junction proteins such as ZO-1, Claudin-5, and Occludin, further enhancing its role in preserving BBB integrity in mice following 8 w of HFD. Similarly, Resveratrol, a naturally occurring polyphenolic compound, has been demonstrated its capacity to fortify BBB tight junctions. Its neuroprotective properties extend beyond just maintaining the BBB; Resveratrol also exhibits antioxidative and anti-inflammatory effects, which are beneficial in addressing the multifactorial aspects of obesity-induced neural damage in mice subjected 8 w of HFD [ 74 ]. However, while these agents show promise, their clinical application faces challenges. The variability in individual responses and potential side effects, such as hypersensitivity reactions with Dapsone, require careful consideration. Future research must focus on optimizing these therapies, possibly through targeted delivery systems or combination therapies, to enhance their protective effects on the BBB while minimizing adverse reactions. Despite these benefits, the challenge with Topiramate lies in its potential side effects, such as cognitive disturbances and weight loss, which might limit its use in certain patient populations. Future research should focus on optimizing its dosage and delivery mechanisms to maximize its therapeutic benefits while minimizing adverse effects. Besides the aforementioned strategies, other pharmacological effects pivotal in managing obesity-induced complications include the modulation of oxidative stress and cellular death, the regulation of metabolic pathways, and the enhancement of neural regeneration, each contributing uniquely towards mitigating the multifaceted challenges posed by obesity.

In conclusion, the emerging therapeutic strategies discussed in this section underscore the complexity and multidimensionality of tackling obesity-induced metabolic syndrome and its neurological implications. From enhancing BBB integrity to addressing oxidative stress, metabolic dysregulation, and promoting neuroregeneration, each approach offers a unique angle in combating the extensive impact of obesity [ 150 , 151 ]. This multifaceted approach not only broadens our understanding but also paves the way for innovative and comprehensive treatments in the ongoing battle against obesity-related neurological disorders. The major experimental therapies are summarized in Table  2 , which presents a curated list of compounds demonstrated to exert protective effects against the adverse consequences of obesity on the brain, particularly focusing on maintaining or restoring BBB integrity. Each compound included has been selected based on empirical evidence from studies highlighting its efficacy in counteracting obesity-induced neurovascular dysfunction.

Conclusion and future directions

The intricate association between obesity and the BBB has been the primary focus of this review. We have delved into the fundamental understanding of BBB dysfunction in the context of obesity, detailing the altered BBB permeability, transport dysfunction, and neuroinflammation, each contributing to a multifaceted pathophysiological landscape that paves the way for obesity-related neurological disorders. Despite the progress made, several gaps persist in our understanding of obesity-induced BBB dysfunction. For instance, more in-depth studies on the temporal relationship between obesity and BBB dysfunction could provide insight into the initial triggers of these changes. Furthermore, it remains unclear whether BBB dysfunction is a universal feature of obesity or if it varies with factors such as the degree and duration of obesity, age, sex, and genetic predisposition. Moreover, the potential reversibility of obesity-induced BBB changes and the optimal strategies for achieving such reversibility warrant exploration.

Recognizing BBB dysfunction’s role in obesity-related neurological diseases holds significant promise for future therapeutic advancements. By better understanding the interactions between BBB dysfunction and neurodegeneration, we may discover new strategies to mitigate or even prevent the deleterious effects of obesity on the CNS. There lies immense potential in targeting the BBB for therapeutic intervention, with the promise of not only alleviating obesity-induced BBB dysfunction but also mitigating its downstream effects, including neuroinflammation and neurodegeneration.

In conclusion, obesity-induced BBB dysfunction represents an area of research with implications extending beyond the realm of obesity to a broad spectrum of neurological disorders. A more comprehensive understanding of obesity’s influence on the CNS would ultimately benefit those affected by obesity and its neurological consequences.

Data availability

No datasets were generated or analysed during the current study.

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This work was supported by the National Natural Science Foundation of China (32170985, 82273923), National Key Research and Development Program of China (2023YFE0202200 and 2021YFA0910000), Guangdong Province Basic and Applied Basic Research Grant (2021B1515120089), Shenzhen Science and Technology Program (JCYJ20210324115800003, ZDSYS20190902093409851 JCYJ20220531100203008), International collaboration project of Chinese Academy of Sciences (172644KYSB20200045), CAS-Croucher Funding Scheme for Joint Laboratories, and Guangdong Innovation Platform of Translational Research for Cerebrovascular Diseases.

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Ziying Feng and Yinzhong Ma wrote the main manuscript text and created the table and figures. Cheng Fang participated in the literature review and data summary. Junlei Chang was the guarantor and revised the manuscript. All authors reviewed the final manuscript.

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Feng, Z., Fang, C., Ma, Y. et al. Obesity-induced blood-brain barrier dysfunction: phenotypes and mechanisms. J Neuroinflammation 21 , 110 (2024). https://doi.org/10.1186/s12974-024-03104-9

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Weight-loss surgery before kidney transplantation improves health and eligibility of patients with obesity and renal failure, Mayo Clinic study finds

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ROCHESTER, Minn. — Laparoscopic sleeve gastrectomy promotes relatively rapid weight loss, reduces obesity-related health issues and improves eligibility for kidney transplantation for patients with advanced chronic kidney disease and obesity , according to new research from Mayo Clinic .

Patients with advanced chronic kidney failure and severe obesity often are not considered for kidney transplantation , but according to a study published in Mayo Clinic Proceedings , sleeve gastrectomy can improve high-risk patients meeting the criteria for transplantation. The findings also show that the surgical weight-loss procedure reduced cardiovascular risks, including diabetes and hypertension.

"In earlier research, we found that conservative weight-loss approaches do not adequately result in significant weight loss in patients with advanced chronic kidney disease," says Aleksandra Kukla, M.D. , a Mayo Clinic transplant nephrologist and the study's first author. "These new findings support the value of surgical gastrectomy for patients with advanced chronic kidney failure, stage 4-5D, to improve general health and access to kidney transplantation."

The retrospective study involved 104 patients with advanced chronic kidney failure and obesity who were treated at Mayo Clinic between 2020 and 2023. Fifty-four underwent laparoscopic sleeve gastrectomy, the most frequently performed surgical weight-loss procedure in patients seeking kidney transplant, and 50 patients opted for a nonsurgical weight-loss approach.

Undergoing sleeve gastrectomy reduced the time for patients to be added to waiting lists for kidney transplantation. It also improved the likelihood of receiving a transplant, with 37% of those who underwent sleeve gastrectomy receiving a transplant within 18 months, versus 10% in the nonsurgical cohort.

The risk of postsurgical complications was low, and the rate of hospitalizations and infections for patients who underwent sleeve gastrectomy was similar to the nonsurgical cohort.

Effective therapy for obesity among patients with advanced chronic kidney disease is understudied, in part because high body mass index (BMI) is often considered beneficial in patients receiving kidney dialysis . "Treatment of obesity in this population has been limited to nonsurgical options in the past," says Tayyab Diwan, M.D. , a Mayo Clinic transplant surgeon and co-author of the study.

More research is needed on the optimal timing of the surgery for kidney transplant candidates, Dr. Diwan says.

About Mayo Clinic Proceedings Mayo Clinic Proceedings is a monthly, peer-reviewed journal that publishes original articles and reviews on clinical and laboratory medicine, clinical research, basic science research and clinical epidemiology. The journal, sponsored by Mayo Foundation for Medical Education and Research as part of its commitment to physician education, has been published for 98 years and has a circulation of 127,000.

About Mayo Clinic College of Medicine and Science Mayo Clinic College of Medicine and Science educates and trains more than 4,000 students, residents and fellows each year in biomedical education. As part of the nonprofit Mayo Clinic academic medical center, the college is supported by Mayo Clinic's world-class clinical expertise, a commitment to academic excellence, and unparalleled research capabilities. The college has five schools: Mayo Clinic Alix School of Medicine , Mayo Clinic Graduate School of Biomedical Sciences , Mayo Clinic School of Graduate Medical Education , Mayo Clinic School of Health Sciences and Mayo Clinic School of Continuous Professional Development .

About Mayo Clinic Mayo Clinic  is a nonprofit organization committed to innovation in clinical practice, education and research, and to providing compassion, expertise and answers to everyone who needs healing. Visit Mayo Clinic News Network  for additional Mayo Clinic news.

Media contact:

• Jay Furst, Mayo Clinic Research and Education Communications, [email protected]
• Mayo Clinic Q&A: Managing migraine: What’s right for me? Hormone therapy: Four things a Mayo Clinic women’s health specialist wants you to know

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