what is the hygiene hypothesis about

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What is Public Health?

Is the Hygiene Hypothesis True?

Did Covid shutdowns stunt kids' immune systems?

Caitlin Rivers

The hygiene hypothesis is the idea that kids need to be exposed to germs in order to develop healthy immune systems. We know that many common viruses did not circulate as widely during the pandemic, thanks to social distancing, masking, and other COVID mitigation measures. Are there downsides to those missed infections?

In this Q&A, Caitlin Rivers speaks with Marsha Wills-Karp, PhD, MHS , professor and chair of Environmental Health and Engineering , about the role of household microbiomes, birth, and vaccines in the development of kids’ immune systems—and whether early exposure really is the best medicine.

This Q&A is adapted from Rivers’ Substack blog, Force of Infection .

I think there’s some concern among parents who have heard about the hygiene hypothesis that there is a downside to all those stuffy noses that didn’t happen [during the COVID-19 pandemic]. Are there any upsides to viral infections? Do they help the immune system in some meaningful way?

I don’t think so.

You mentioned the hygiene hypothesis, which was postulated back in the ‘80s. German scientists noticed that families with fewer children tended to have more allergic disease. This was interpreted [to mean] that allergic disease was linked to experiencing fewer infections. I have explored this idea in my research for a couple of decades now.

This phenomenon has helped us to understand the immune system, but our interpretation of it has grown and expanded—particularly with respect to viruses. Almost no virus is protective against allergic disease or other immune diseases. In fact, infections with viruses mostly either contribute to the development of those diseases or worsen them.

The opposite is true of bacteria. There are good bacteria and there are bad bacteria. The good bacteria we call commensals . Our bodies actually have more bacterial cells than human cells. What we’ve learned over the years is that the association with family life and the environment probably has more to do with the microbiome. So one thing I would say is sanitizing every surface in your home to an extreme is probably not a good thing. Our research team showed in animals that sterile environments don’t allow the immune system to develop at all. We don’t want that.

What does contribute to the development of the immune system, if not exposure to viruses?

There are a number of factors that we’ve associated with the hygiene hypothesis over the last 20 years, and these exposures start very early in life. Cesarean sections, which do not allow the baby to travel through the birth canal and get exposed to the mother’s really healthy bacterial content, is a risk factor for many different immune diseases. Getting that early seeding with good bacteria is critical for setting up the child going forward. Breastfeeding also contributes to the development of a healthy immune system.

There are other factors. Our diets have changed dramatically over the years. We eat a lot of processed food that doesn’t have the normal components of a healthy microbiome, like fiber. These healthy bacteria in our gut need that fiber to maintain themselves. They not only are important for our immune system but they’re absolutely critical to us deriving calories and nutrients from our food. All these things contribute to a healthy child.

We’ve also noticed that people who live on farms have fewer of these diseases because they’re exposed to—for lack of a better term—the fecal material of animals. And what we have found is that it’s due to these commensal bacteria. That is one of the components that help us keep a healthy immune system. Most of us will probably not adopt farm life. But we can have a pet, we can have a dog.

I think all the pet lovers out there will be pleased to hear that.

There’s a lot of evidence that owning a pet in early childhood is very protective.

What about the idea that you need to be exposed to viruses in early life because if you get them as an adult, you’ll get more severely ill? We know that’s true for chickenpox, for example. Do you have any concerns about that?

We should rely on vaccines for those exposures because we can never predict who is going to be susceptible to severe illness, even in early childhood. If we look back before vaccines, children under 4 often succumbed to infections. I don’t think we want to return to that time in history.

Let me just give you one example. There’s a virus called RSV, it’s a respiratory virus. Almost all infants are positive for it by the age of 2. But those who get severe disease are more likely to develop allergic disease and other problems. So this idea that we must become infected with a pathogenic virus to be healthy is not a good one.

Even rhinovirus, which is the common cold, most people recover fine. But there’s a lot of evidence that for somebody who is allergic, rhinovirus exposures make them much worse. In fact, most allergic or asthmatic kids suffer through the winter months when these viruses are more common.

And that’s particularly salient because there is a lot of rhinovirus and enterovirus circulating right now.

From my point of view, right now, avoiding flu and COVID-19 is a priority. Those are not going to help you develop a healthy immune response, and in fact, they can do a lot of damage to the lungs during that critical developmental time. Data [show] that children that have more infections in the first 6 months to a year of life go on to have more problems.

It’s always surprising to me when I look at the data of the fraction of time that young children spend with these common colds—and this is pre-pandemic—it’s not uncommon for kids to be sick 50% of the time. That feels right as a parent, but it’s startling.

The other thing people don’t know is that the GI tract is where you get tolerized to all of your foods, allergens and things. Without those healthy bacteria in your gut, you can’t tolerate common allergens.

How does that relate to the guidance that’s changed over the years—that you should withhold peanuts in early life and now you’re supposed to offer them in early life?

The guidance to delay exposure to peanuts didn’t consider the fact that oral exposure to peanuts was not the only exposure kids were getting. There were peanut oils in all kinds of skin creams and other things. So kids got exposed through their skin, but they had no gut protection—and the GI tract is important for a tolerant system. If you have a healthy immune response, you get tolerized in early life.

This concept is a little bit different for those families who may already have a predisposition to allergies. But for the general public, exposure is key to protecting them in early life.

I think some parents look at the guidance that you should now offer peanuts in early life and say, “Are we not doing that with rhinovirus by masking kids or improving ventilation?” How should people think about the development of the immune system for food allergies compared to infections?

The thing about rhinoviruses is that after recovering, you’re not protected from the next infection. There is no real immune protection there. Most of us suffer from colds throughout our whole life. Like I said, bacterial exposure is what’s key to priming the immune response.

Also, we forget that a lot of kids die from the flu. Unlike COVID-19, where younger kids are not quite as susceptible to severe illness, that’s not true for flu. RSV, too, can be quite severe in young children and older adults.

Caitlin Rivers, PhD, MPH , is a senior scholar at the Johns Hopkins Center for Health Security and an assistant professor in Environmental Health and Engineering at the Johns Hopkins Bloomberg School of Public Health.

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What Is the Hygiene Hypothesis?

Many parents believe that their children must be kept in an environment that is as clean as possible, but some research suggests that being exposed to what many would call unclean conditions is good for a child's immune system. Research has indicated that children who are kept in very clean environments have a higher rate of hay fever, asthma and a wide range of other conditions. This is what is called the hygiene hypothesis.

The hygiene hypothesis was first introduced in the late 1980s by David P. Strachan, a professor of epidemiology, in the British Medical Journal. Strachan found that children in larger households had fewer instances of hay fever because they are exposed to germs by older siblings. This finding led to further research that suggests a lack of early childhood exposure to less than pristine conditions can increase the individual's susceptibility to disease.

For example, in the late 1990s, Dr. Erika von Mutius, a health researcher, compared the rates of allergies and asthma in East Germany and West Germany, which unified in 1999. Her initial hypothesis was that East German children, who grew up in dirtier and generally less healthful conditions, would have more allergies and suffer more from asthma than their Western counterparts. However, her research found the opposite: children in the polluted areas of East Germany had lower allergic reactions and fewer cases of asthma than children in West Germany.

Further research has found that children in developing areas of the world are less likely to develop allergies and asthma compared with children in the developed world.

Building the immune system

The idea is simple. When babies are inside the womb they have a very weak immune system because they are given protection by their mother's antibodies. When they exit the womb, though, the immune system must start working for itself. For the immune system to work properly, it is thought that the child must be exposed to germs so that it has a chance to strengthen, according to the U.S. Food and Drug Administration (FDA).

The idea is similar to the training of a body builder. For a body builder to be able to lift heavy objects, the muscles must be trained by lifting heavier and heavier objects. If the body builder never trains, then he will be unable to lift a heavy object when asked. The same is thought to be true for the immune system. In able to fight off infection, the immune system must train by fighting off contaminants found in everyday life. Systems that aren't exposed to contaminants have trouble with the heavy lifting of fighting off infections.

Mutius hypothesized that the reason children who are not exposed to germs and bacteria are sicklier is due to how the human immune system evolved. She thinks there are two types of biological defenses. If one of the defense systems isn't trained or practiced enough to fight off illness, the other system overcompensates and creates an allergic reaction to harmless substances like pollen.

Research by other scientists has found similar results. Exposure to germs triggered an internal inflammatory response in children who were raised in cleaner environments, leading to ailments such as asthma, according to a 2002 article in Science magazine.

One researcher has personal experience has leads him to back the hygiene hypothesis. "I believe that there is a role in the development of a child's immunity exposure to various germs and a vast microbiome diversity," said Dr. Niket Sonpal, an assistant professor of clinical medicine at Touro College of Osteopathic Medicine, Harlem Campus. "I was born in India but moved to the U.S. and went to college in Virginia and medical school in Europe. I am sure that the vast change in environment has played a role in my immunity. How has it? I don't think we know just yet."

In 1997, some began to question if there is a correlation between the hygiene hypothesis and vaccinations. The number of children getting vaccinations was going up, but so were the number of children afflicted with allergies, eczema and other problems. Could depriving the developing immune system of infections using vaccines cause the immune system to eventually attack itself and cause autoimmune diseases like asthma and diabetes? This is a highly contested issue.

Three studies conducted in the 1990s showed that vaccines had no correlation with children developing allergies and other ailments later in life. In fact, vaccinations may help prevent asthma and other health problems other than the diseases they were intended to prevent, according to The National Center for Immunization Research and Surveillance . The idea that vaccinations can cause health problems does not consider the fact that children, whether vaccinated or not, are still exposed to pathogens that help build the immune system. These pathogens also have no relation to the diseases that the vaccines prevent.

The conflict between cleanliness and exposure can leave parents feeling confused. There are many microbes that can make children very sick, such as such as respiratory syncytial virus (RSV), E.coli and salmonella. So cleaning the home is still very important. What should children be exposed to and what should they be protected from?

The CDC recommends regularly cleaning and disinfecting surfaces in the home, especially when surfaces have been contaminated by fecal matter or meat or have come in contact with those who have a virus. Children are also encouraged, though, to play outside , even if they may get dirty in the process. This balancing act may prove to help children stay healthy while still developing a healthy immune system.

Sonpal thinks that the healthy growth of the immune system isn't just about coming in contact with dirt. It also has to do with what foods are consumed, what kind of environments the person grows up in and intrinsic genetics coupled with physical activity levels. Harvard Medical School noted that getting plenty of sleep, avoiding cigarette smoke, drinking in moderation and controlling blood pressure also all play a part in a healthy immune system.

Additional Resources

Clinical & Experimental Immunology: The 'Hygiene Hypothesis' for Autoimmune and Allergic Diseases: An Update
Mayo Clinic: Early germ exposure prevents asthma?
U.S. National Library of Medicine: The Hygiene Hypothesis and home hygiene

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Asthma: The Hygiene Hypothesis

What do clean houses have in common with childhood infections.

One of the many explanations for asthma being the most common chronic disease in the developed world is the “hygiene hypothesis.” This hypothesis suggests that the critical post-natal period of immune response is derailed by the extremely clean household environments often found in the developed world. In other words, the young child’s environment can be “too clean” to pose an effective challenge to a maturing immune system.

According to the “hygiene hypothesis,” the problem with extremely clean environments is that they fail to provide the necessary exposure to germs required to “educate” the immune system so it can learn to launch its defense responses to infectious organisms. Instead, its defense responses end up being so inadequate that they actually contribute to the development of asthma.

Scientists based this hypothesis in part on the observation that, before birth, the fetal immune system’s “default setting” is suppressed to prevent it from rejecting maternal tissue. Such a low default setting is necessary before birth—when the mother is providing the fetus with her own antibodies. But in the period immediately after birth the child’s own immune system must take over and learn how to fend for itself.

The “hygiene hypothesis” is supported by epidemiologic studies demonstrating that allergic diseases and asthma are more likely to occur when the incidence and levels of endotoxin (bacterial lipopolysaccharide, or LPS) in the home are low. LPS is a bacterial molecule that stimulates and educates the immune system by triggering signals through a molecular “switch” called TLR4, which is found on certain immune system cells.

The science behind the hygiene hypothesis

The Inflammatory Mechanisms Section of the Laboratory of Immunobiochemistry is working to better understand the hygiene hypothesis, by looking at the relationship between respiratory viruses and allergic diseases and asthma, and by studying the respiratory syncytial virus (RSV) in particular.

What does RSV have to do with the hygiene hypothesis?

RSV is often the first viral pathogen encountered by infants.
RSV pneumonia puts infants at higher risk for developing childhood asthma. (Although children may outgrow this type of asthma, it can account for clinic visits and missed school days.)
RSV carries a molecule on its surface called the F protein, which flips the same immune system “switch” (TLR4) as do bacterial endotoxins.

It may seem obvious that, since both the RSV F protein and LPS signal through the same TLR4 “switch,” they both would educate the infant’s immune system in the same beneficial way. But that may not be the case.

The large population of bacteria that normally lives inside humans educates the growing immune system to respond using the TLR4 switch. When this education is lacking or weak, the response to RSV by some critical cells in the immune system’s defense against infections—called “T-cells”—might inadvertently trigger asthma instead of protecting the infant and clearing the infection. How this happens is a mystery that we are trying to solve.

In order to determine RSV’s role in triggering asthma, our laboratory studied how RSV blocks T-cell proliferation.

Studying the effect of RSV on T-cells in the laboratory, however, has been very difficult. That’s because when RSV is put into the same culture as T-cells, it blocks them from multiplying as they would naturally do when they are stimulated. To get past this problem, most researchers kill RSV with ultraviolet light before adding the virus to T-cell cultures. However we did not have the option of killing the RSV because that would have prevented us from determining the virus’s role in triggering asthma.

Our first major discovery was that RSV causes the release from certain immune system cells of signaling molecules called Type I and Type III interferons that can suppress T-cell proliferation (Journal of Virology 80:5032-5040; 2006).

The hygiene hypothesis suggests that a newborn baby’s immune system must be educated so it will function properly during infancy and the rest of life. One of the key elements of this education is a switch on T cells called TLR4. The bacterial protein LPS normally plays a key role by flipping that switch into the “on” position.

Prior research suggested that since RSV flips the TLR4 switch, RSV should “educate” the child’s immune system to defend against infections just like LPS does.

But it turns out that RSV does not flip the TLR switch in the same way as LPS. This difference in switching on TLR, combined with other characteristics of RSV, can prevent proper education of the immune system.

One difference in the way that RSV flips the TLR4 switch may be through the release of interferons, which suppresses the proliferation of T-cells. We still do not know whether these interferons are part of the reason the immune system is not properly educated or simply an indicator of the problem. Therefore, we plan to continue our studies about how RSV can contribute to the development of asthma according to the hygiene hypothesis.

Further research

This finding that Type I and Type III interferons can mediate the suppression of T-cells caused by RSV generated two significant questions that our laboratory is now addressing:

Interferons are important molecules that enhance inflammation, so why--in the context of RSV--do they suppress T-cells?
Interferons are clearly not the only way RSV suppresses T-cells. What are the other mechanisms that may depend upon T-cells coming in direct contact and communicating with other immune cells?

Related Research

Assessing the Mechanism of Immunotherapy for Allergy and Allergic Asthma: Effect of Viral Respiratory Infections on Pathogenesis and Clinical Course of Asthma and Allergy Ronald Rabin, MD

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Review Article
Published: 16 October 2017

The hygiene hypothesis in autoimmunity: the role of pathogens and commensals

Jean-François Bach 1 , 2 , 3

Nature Reviews Immunology volume 18 , pages 105–120 ( 2018 ) Cite this article

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Autoimmune diseases
Toll-like receptors

The initial application of the hygiene hypothesis for autoimmune diseases proposed in the early 2000s has been confirmed and consolidated by a wealth of published data in both animal models and human autoimmune conditions.

The hygiene hypothesis probably explains the uneven geographical distribution of autoimmune diseases in the world. Individuals migrating from countries with low incidence of autoimmune diseases to countries with high incidence develop the disease with the frequency of the host country, provided that migration occurred at a young age and under a threshold that varies according to the disease.

Pathogenic bacteria, viruses and parasites are often endowed with strong protective effects on autoimmunity even when infection occurs late after birth.

Gut commensal bacteria may also have a protective role in autoimmunity when administered early in life.

Pathogens, parasites and commensals essentially act by stimulating immune regulatory pathways, implicating the innate and the adaptive immune system. Importantly, the effect is seen with both living organisms and their derivatives or purified extracts.

Both pathogens and commensals stimulate pattern recognition receptors, including Toll-like receptors (TLRs) to protect against autoimmunity. This effect may be mimicked by TLR agonists acting through pharmacological stimulation or desensitization of the target receptor.

The incidence of autoimmune diseases has been steadily rising. Concomitantly, the incidence of most infectious diseases has declined. This observation gave rise to the hygiene hypothesis, which postulates that a reduction in the frequency of infections contributes directly to the increase in the frequency of autoimmune and allergic diseases. This hypothesis is supported by robust epidemiological data, but the underlying mechanisms are unclear. Pathogens are known to be important, as autoimmune disease is prevented in various experimental models by infection with different bacteria, viruses and parasites. Gut commensal bacteria also play an important role: dysbiosis of the gut flora is observed in patients with autoimmune diseases, although the causal relationship with the occurrence of autoimmune diseases has not been established. Both pathogens and commensals act by stimulating immunoregulatory pathways. Here, I discuss the importance of innate immune receptors, in particular Toll-like receptors, in mediating the protective effect of pathogens and commensals on autoimmunity.

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Acknowledgements

The laboratory of the author was supported by an advanced grant from the European Research Council (ERC, Hygiene N°: 250290).

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Jean-François Bach

INSERM U1151, Institut Necker-Enfants Malades, Hôpital Necker-Enfants Malades, Paris, France

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PowerPoint slides

Powerpoint slide for fig. 1, powerpoint slide for fig. 2, powerpoint slide for table 1, powerpoint slide for table 2, powerpoint slide for table 3.

A genetic predisposition to the cumulative development of common allergies, for example, atopic dermatitis and allergic asthma. Atopy involves phenomena of cutaneous or general hypersensitivity to allergens.

A hypothesis that postulates that an increased frequency of infections contributes to a decrease in autoimmune and allergic diseases.

An inbred mouse line that spontaneously develops an autoimmune syndrome including insulin-dependent diabetes mellitus (IDDM or type 1 diabetes).

A digestive tract disorder provoked by eating contaminated food or drinking contaminated water. In the context of our discussion, it is a self-limited pathology that illustrates the presence of a basic health environment.

Autoantibodies to various β-cell-specific autoantigens that are markers of the destruction of insulin-producing β-cells, which is the hallmark of insulin-dependent diabetes mellitus (IDDM or type 1 diabetes).

An imbalance of the microbial flora that most frequently affects the digestive tract. Dysbiosis can also be detected in other 'barrier' organs such as the skin, the lungs or the vagina.

The metabolome consists of all signalling molecules (for example, metabolites and hormones) detected in a biological sample. The metabolome thus defines a given physiological or pathological state and is therefore dynamic.

Mice born by hysterectomy under sterile conditions and raised in isolators to guarantee an environment totally devoid of pathogenic and commensal germs.

(EAE). A demyelinating allergic encephalomyelitis produced by the injection of brain tissue or purified proteins of the nervous system or their derived peptides in the presence of an adjuvant.

Germ-free mice whose intestinal microflora is reconstituted by a single commensal bacterium (monocolonized mice).

Gut commensal bacteria available as single or combined species delivered orally and putatively endowed with a health benefit.

The competition for recognition of the cognate antigen for soluble factors (cytokines) driving the proliferation and differentiation of antigen-specific lymphocytes.

Islet transplants between syngeneic (genetically identical) donor and recipient individuals, which therefore does not give rise to allograft rejection. These grafts performed in diabetic non-obese diabetic mice provide a robust model to test for recurrence of the autoimmune disease.

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Bach, JF. The hygiene hypothesis in autoimmunity: the role of pathogens and commensals. Nat Rev Immunol 18 , 105–120 (2018). https://doi.org/10.1038/nri.2017.111

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April 7, 2011

Can It Be Bad to Be Too Clean?: The Hygiene Hypothesis

Johns Hopkins School of Medicine researcher Kathleen Barnes talks about the hygiene hypothesis, which raises the possibility that our modern sterile environment may contribute to conditions such as asthma and eczema

By Steve Mirsky

Johns Hopkins School of Medicine researcher Kathleen Barnes talks about the hygiene hypothesis , which raises the possibility that our modern sterile environment may contribute to conditions such as asthma and eczema.

Podcast Transcription

Steve: Welcome to Science Talk , the more of less weekly podcast of Scientific American , posted on April 6th, 2011. I am Steve Mirsky. This week on the podcast:

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Barnes: The hypothesis is that as we make the shift from dirt to sterile that you're changing the direction of your immune response. This causes diseases.

Steve: That's Kathleen Barnes. We'll hear from her, and we'll test your knowledge of some recent science in the news. Kathleen Barnes studies what's called the hygiene hypothesis at the Johns Hopkins School of Medicine in Baltimore. She presented some of her research at the recent meeting of the American Association for the Advancement of Science in Washington, D.C., after which we sat down to chat.

Steve: First, tell me what is the hygiene hypothesis, for people who haven't heard of it?

Barnes: So, the hygiene hypothesis, I guess, simply stated is this notion that as human society has morphed from developing environment, or what we consider a developing world environment, into the developed world, there have been radical changes in our environment; changes associated with the size of families, so going from many to fewer siblings. The idea being that with fewer children in the house, there's less opportunity for exposure to viruses. The idea that we move from a rural to an urban environment; that we have moved from that situation where we're exposed to microbes—one of the best examples in asthma being the idea that we're exposed to endotoxins that is a byproduct of the livestock and farms—to moving to an environment that's more sterile, where we don't have such exposures. The notion that as we move from a developing to a developed environment, we have less exposure to microbes in general. We treat every symptom with antibiotics; we've changed our gut microflora with the diets that we eat.

Steve: We use antibacterial soap and antibacterial surface cleaners in the house.

Barnes: Exactly, yeah, the idea is sterile is good. Sterile is healthy.

Steve: That's the hygiene; what's the hypothesis part?

Barnes: The hypothesis is that as we make the shift from dirt to sterile that you are changing the direction of your immune response. And so in the context of asthma, and frankly in other autoimmune diseases and diseases of inflammation, it's this imbalance from that side of our immune response that we believe evolved to protect us against things like bacteria and viruses and malarial parasites to the other side of our immune system that, frankly, when it's revved up causes diseases like allergies and some of these other diseases of inflammation. So it's really this imbalance between these two sides of our immune system, both which were designed to do something good for us; but when it's not equal, when it's imbalanced, we're going to have too much of one disease versus another.

Steve: So without the exposure to these environmental challenges, we wind up trading one set of conditions for a different set of conditions or illnesses.

Barnes: Exactly. And the whole, the notion of the epidemiological transition is that we've gone from a situation in our distant past, where we're exposed to lots of microbes—but we also, to be frank, we died from a lot of these diseases; so, it's not to romanticize our past, certainly these microbes were able to kill us and cause great consternation in city-state populations. But the idea is that some balance protects you on the one hand from some of those.

Steve: Yeah, I mean, nobody wants to go back to the days when we didn't have clean drinking water. Arguably clean drinking water is the single most important public health development in the history of humanity. And so we're not dying so much in the developed world of dysentery and other conditions of unsanitary drinking water, and we don't have to drink alcohol all day to make sure that we're not drinking dangerous liquids; but you know, dangerous in a different way and people used to die younger because they were getting infection and you would die from it. And, I mean, that still those happen today but, you know, fortunately we do have antibiotics and other things. So we're not arguing to go back to that. But we have realized that people have teased out the fact that maybe some of the now epidemic asthma rates, for example, are related to the fact that kids when they are growing up and even before they're born are not being challenged, their immune systems are not being challenged the way that we evolved.

Barnes: So I was going to throw that very example out, sort of, the classic example or the classic notion is that an individual's propensity to be more upregulated on one side of their immune system—say Th1 versus their Th2, the Th1 side being that side of our immune system that we believe evolved to protect us against things like the bacteria and the viruses and microbes; versus Th2 which served a very fundamental purpose in an environment where one was exposed to worms. But we're not exposed to worms anymore, so that side doesn't serve as much of a purpose, and we know from very sophisticated studies that infants that are born to mothers in the, sort of, with the, sort of, sterile environment, infants are born with the predisposition to be Th2 skewed. And there is a reason for that. During the neonatal period, it's important for the mother not to reject the fetus as the fetus is developing and so the mother's immune response is slightly tilted towards this Th2 to not treat the fetus as a microbe, if I can put it that bluntly.

Steve: Which is really a good thing.

Barnes: (laughter) At the time that when the infant is born, so the infant is born with a slight Th2 preference over the Th1, because that was the intrauterine environment. The thinking is that when exposed to some bacteria, some viruses, it sort of shifts this back into an equilibrium. But unfortunately in our current environment, where everything is sterile, we tend to forego breastfeeding and feed our infants formula from sterile water and so on and so forth, there are fewer siblings at home, we're not really giving these infants the chance to equalize, if you will, that immune response.

Steve: So what are some of the actual studies? What are your research interests that have confirmed that this situation exists out there?

Barnes: So, there have been a number of studies in the field of asthma, studies that have not necessarily been our own certainly include the German farming studies by Erika von Mutius and others showing that children who lived in very close proximity to livestock, and we know are exposed to lots of bacteria, for example, from the livestock are less likely to have asthma and allergies. There have been beautiful studies showing that children who go to daycare very early in life, who are therefore exposed to more rhinovirus and virus in general tend to have fewer asthma and allergies as they grow up. In our own work, we've taken a closer look at that exposure to that bacteria, the gram-negative bacteria we call endotoxin, which is ubiquitous, it's around us all the time; but it's certainly higher in some places than others and endotoxin we know doesn't just come from livestock, endotoxin comes from diesel exhaust. So there have been some various nice studies showing elevated levels of endotoxins in regions where folks live in close proximity to traffic. Right up the road in the Baltimore tunnel, there's some of the highest endotoxin levels that have ever been recorded.

Steve: How does that it get in the diesel exhaust?

Barnes: It's part of the particulate matter.

Steve: It's just picking it up from the environment and pluming it out?

Barnes: Exactly, we were interested in testing that theory that with higher levels of endotoxin, there would be lower levels of asthma and allergy. When we measure endotoxin in the tropical environment it looks very different than it does in a developed environment such as here. It's much higher and it's probably higher for a variety of reasons. In our one particular study that we've done in Barbados, folks live very close to the road, and they're exposed to very high levels of diesel exhaust, and we believe that pollution has contributed over time to an ever increasing prevalence of asthma in that society. When we measure endotoxin in the homes of these folks, it's very, very high but they have a lot of asthma and allergy, so I think that's telling us that the hygiene hypothesis is not a black and white hypothesis, that there are a lot of complexities to this. And for me personally it tells me that there are also genetic underpinnings. So it's not just about exposure to the environment, just as it's not just about having a particular mutation that puts you at risk of developing disease, but it's the interaction of those two factors—genes and environment that will probably help us have a better understanding of the Hygiene hypothesis.

Steve: It's definitely multifactorial, but when you deal with large enough populations you can start to tease out these kinds of relationships.

Barnes: Absolutely. Having the opportunity to study very large populations allows you to stratify folks based on exposure to factor A and B; allows you to stratify on not just one genetic polymorphism but many polymorphisms. So there is much to be gained from these very large population studies. And I frankly think that to get a better handle on the role of the hygiene hypothesis not just an asthma and allergic disease but any of these other complex diseases, the real key also are longitudinal studies, birth cohort studies, where we've been able to track an individual from the time he or she is born, measure various environmental exposures along the way, and then compare that to their genetic background.

Steve: So, we're not going to advise people to, oh go get the helminth worm infection, or you know, go roll around in the dirt on a farm nearby with your kids; nobody is going to advise that. So what is the practical application going to be of this kind of knowledge?

Barnes: Right, so it's very tempting, it's very tempting to come up with a conclusion that being exposed to a lot of dirt is good for your health or that being exposed to and infested with worms is good for your health. We wouldn't advocate either of those, but what I think the real value in this science really is, is if we can understand what it is about those microbes, and in the case of the parasite, what is it about the protein within the parasite that elicits this response to the parasite, either protective or conferring risk of the disease? If we could put our finger on that particular molecule we could develop better therapeutics for people. We could, you're not going to advocate giving an individual worms to cure their asthma or to cure their autoimmune disease. But you could come up with a drug that has some part of that protein that elicits this biological response and give that to the individual therapeutically.

Steve: How did you wind up working on this subject? Did you start way back in grad school? Or I don't mean way back.

Barnes: (laughter) No, you can say that because it's true.

Steve: Okay, or was it something that came along in the middle of your academic career?

Barnes: My work has really evolved truly over several decades. So as a graduate student, I was very interested, as a graduate student in medical anthropology, in differences across human populations and our response to environmental factors that confer risk of disease; and schistosomiasis was one disease I was particularly interested in.

Steve: This is a worm-borne disease.

Barnes: Schistosomiasis is a worm-borne disease; it's referred to as a helminth and it's spread to the human host through infested waters. Schistosomiasis typically doesn't carry a very high mortality rate. It can be debilitating for those individuals who can't mount an appropriate response against the worm. But my interest really started at that point in time with this interest in how and why we respond to different factors such as parasites, and truly that dovetailed in to what was a growing interest in the mid '80s of why there was an increase in asthma and allergic disease; and the hypothesis had been put forth that the IgE antibody that we all make but typically in very low quantities, had only been discovered in 1968. So, it was a relatively new immunological molecule that we knew was important in our immune system, and we knew it was very important in causing risk to asthma and other allergies like eczema and hay fever. At the same time, we began to appreciate that this IgE molecule was also protective against extracellular parasites. So, I was interested in that co-association with this molecule IgE. Over time, my research really focused more on identifying genetic determinants for asthma and allergies. I put the schistosomiasis studies aside. And then about 10 years ago, I had the opportunity to join forces with colleagues and immunologists in Brazil where schistosomiasis is still quite endemic and; in fact it's one of the last strongholds for schistosomiasis in the western hemisphere. And it just provided a really unique opportunity to test the hypothesis that some of these asthma genes that we had identified might also be important in schistosomiasis.

Steve: This is, you know, the hackneyed question, but where do you think things might be in another 10 or 15 years?

Barnes: I think that the hygiene hypothesis particularly and a sort of Darwinian approach in the way we think about medicine in general; that is how did we develop heart disease? How did we develop allergic diseases? How did we develop inflammatory bowel disease? We know as anthropologists that traditional foraging societies didn't have these diseases, and we know that it is not just because they didn't live past the age of 40. They simply didn't develop many of these complex chronic diseases that we experience now. So, I think this new way of approaching the pathology behind these different diseases is opening our minds and understanding, or elucidating new pathways that we didn't think about before. And I am very hopeful that with the better understanding of the pathologies that contribute to these diseases, with a better understanding of how a genetic mutation long ago that protected us against one disease now coincidentally causes another disease, will absolutely help us to develop better therapeutic targets; and not just treat these diseases but also predict who is going to be at greatest risk for disease. And once we know enough about all the environmental factors that go into causing a disease, we as medical folk can give better advise to patients about what they need to avoid or how they need to modify their lifestyle so that they can live longer and healthier lives.

Steve: This host-pathogen interaction is really so fascinating to study because you're dealing with this co-evolutionary situation but the rates are so different. So, we're practically standing still compared to the rates at which the pathogens get to evolve. And it's just I think, it's one of the most fascinating fields to be studying right now.

Barnes: It's indeed an exciting field, and I think it's a very important perspective that where we are now in the 21st century with the diseases we face, is such a recent moment in our human evolutionary time. And frankly that's one of the reasons why we've been particularly interested in focusing on diseases for which there is tremendous ethnic and racial disparities. Because it really isn't until very recently in time that we see the admixture, the mixing of individuals of different ancestral backgrounds. And it actually provides us a great opportunity to try to tease out at least from a genetic epidemiology perspective what mutations might have evolved that were selective or advantageous in one particular environment that individuals have carried with them as they've migrated to new parts of the world; and basically admix with other populations for which there might not have been selective advantage for having a mutation and therefore no mutation at all. And so by studying populations from a more ancient background, if I could, we believe that because our gene pool simply hasn't had enough time to change this rapidly, it's a great test tube experiment, if you will.

Steve: Natural experiment….

Barnes: A natural experiment to say, okay just yesterday in the time clock of human evolution you lived in an environment where if you have this mutation you will better off than the next guy who didn't have it, because it protected you against, for example, parasites. But now you've moved to another part of the world, and you're not exposed to those parasites anymore, but you still have that mutation that was adaptive back in that environment. Since you're not there anymore and you're exposed to new environmental factors, does that place you at risk for diseases that your ancestors wouldn't have thought about?

Steve: It's really fascinating. And we may be living in a unique window of time to do those studies, because with the mixing of all the different human population groups, in another couple of hundred years, it may be impossible to do those kinds of studies.

Barnes: So this is a really important point that right now it's a really terrific opportunity for us to try to tease out what about our human genome, based on our bio-geographical past, can we look at to try to explain why in contemporary times we have disease X. But this will change over time because with that mixture, there are simply diminishing of the benefit of having these mutations that might have been adaptive in a previous time. So yes it is a unique opportunity. And I guess I will just add to that the other opportunity, if we can call it that, is that with globalization and rapid changes in these places that we perform these studies where we are looking at more traditional ways of living and then comparing that to the way we live here in the United States, for example; so even within our Brazil study where we've studied parasitic disease, certainly the public health goal is to eradicate parasitic disease in these populations. And that is the first and foremost priority. But as that happens, we will have less and less opportunity to understand what it is about our past that brought us to where we are now in terms of these genetic polymorphisms that might have served some beneficial purpose.

Steve: Right. We're in no way saying not to try to make this situation better. We're just saying that we better do these studies now before we do accomplish what we hope to accomplish.

Barnes: Exactly. We can learn so much from our past by comparing people who live in different environments under different conditions and in different degrees of development, and I think that comes back to the hygiene hypothesis—that it is a unique opportunity to compare populations with different degrees of development to try to hone in on those specific factors that were emblematic of our past but are simply not part of our modern lifestyle.

Steve: Now it's time to play TOTALL……. Y BOGUS. Here are four science stories; only three are true. See if you know which story is TOTALL……. Y BOGUS.

Story 1: In the newest version of the popular Madden NFL football video game players can get concussions.

Story 2: The late Elizabeth Taylor probably had a FOXC2 gene mutation that affects embryonic development. Story 3: Wind turbines are becoming a huge killer of birds, taking down some 20 million annually.

And story 4: Growing salamander embryos have been found to have algae living happily inside their tissues. While you think about those stories: Do you believe in the effectiveness of subliminal messages? I think the idea that such messages can really work has pretty much been discredited, but who knows.

Hey, you're time is up.

Story 1 is true. In the new Madden Football game, players can get concussed and will be unavailable for the remainder of the game. So as in real football the object of the game will be to give the opposing team's quarterback a concussion.

Story 2 is true. Liz Taylor probably did have the FOXC2 gene mutation which conferred upon her a double role of her famous thick eyelashes.

And story 4 is true. Growing salamander embryos have been found to harbor algae within their tissues. Researchers think the algae get nitrogen rich waste products and the salamanders get oxygen. It's a winner-winner salamander dinner situation. For more check out the April 5th episode of the daily SciAm, podcast, 60-Second Science .

All of which means that Story 3 about wind turbines killing 20 million birds annually is TOTALL……. Y BOGUS. Now what is true is that the bird death toll from turbines is significant—about 440,000 birds per year according to the US Fish and Wildlife Service, and it's an issue that needs to be addressed as wind power hopefully becomes more of an energy contributor. But the real bird killer is on your couch. The American Bird Conservancy says that domestic cats kill about 250 million birds each year, a figure matched by feral cats; which means that wind turbines right now get less than a 10th of a percent as many birds as cats do.

That's it for this episode. Get your science news at www.ScientificAmerican.com, where you can check out the Daily Science Agenda, which features what you need to know now. For example: How does a 737 lose its fuselage in mid-flight? Find out at our Web site safely on the ground and follow us on Twitter, where you'll get a tweet about each new article posted to our Web site. Our Twitter handle is @sciam. For Science Talk , the podcast of Scientific American , I'm Steve Mirsky. Thanks for clicking on us. Try the Scientific American smart phone app.

The hygiene hypothesis: How being too clean might be making us sick

by Joseph Stromberg

Over the past few decades, doctors have arrived at a counterintuitive hypothesis about our modern, ultra-sanitized world. Too much cleanliness may be causing us to develop allergies, asthma, inflammatory bowel diseases, and other autoimmune disorders.

The idea is that for many children in the wealthy world, a lack of exposure to bacteria, viruses, and allergens prevents the normal development of the immune system, ultimately increasing the chance of disorders within this system down the road. This is called the hygiene hypothesis .

a lack of exposure to bacteria, viruses, and allergens may prevent the normal development of the immune system

“A child’s immune system needs education, just like any other growing organ in the human body,” says Erika von Mutius, a pediatric allergist at the University of Munich and one of the first doctors to research the idea. “The hygiene hypothesis suggests that early life exposure to microbes helps in the education of an infant’s developing immune system.” Without this education, your immune system may be more prone to attacking the wrong target — in the case of autoimmune diseases, yourself.

It's still a matter of active debate among scientists, but e vidence for the idea has been slowly accumulating over time, both in humans and animal subjects. It's been cited as an explanation for why allergy and asthma rates are so much higher in wealthy countries, and m ost recently, a study published last year found that babies who grow up in houses with higher levels of certain bacteria — carried on cockroach, mouse, and cat dander — are less likely to develop wheezing and asthma by the age of three.

(However, it’s important to note that despite the claims of some anti-vaccine activists, there’s absolutely no evidence that not getting vaccinated has similar benefits.)

How could this kind of filth possibly make us healthier? Here’s an explanation of the hygiene hypothesis.

How doctors got the idea that dirt could make us healthy

(REMY GABALDA/AFP/Getty Images)

Obviously, the basic sanitary practices we've developed as a society over the past few centuries — such as building infrastructure to remove garbage and sewage from cities — have provided all sorts of benefits. They're a huge part of the reason so few Americans get infectious diseases like cholera or typhoid nowadays.

asthma, hay fever, and other allergies have become much more common as we've become more sanitary

But researchers have found that a few specific autoimmune diseases — asthma, hay fever , inflammatory bowel diseases, and various allergies — have become much more common as we've become more sanitary, and are much more prevalent in the wealthy world than the developing one.

In the late 1980s, when studying childhood allergies in East and West Germany, British epidemiologist David Strachan began to suspect there was a connection. In the dirtier, more polluted, less wealthy cities of East Germany, he found, children had much lower rates of hay fever and asthma than in the cleaner, richer cities of West Germany.

To explain this, he looked at all sorts of lifestyle differences — and found that West German children were much less likely to spend time in day care centers, around other kids, than East German children. He proposed that their reduced exposure to bacteria and other antigens, normally acquired from other children, somehow affected their immune systems, leading to their increased chance of developing the autoimmune diseases.

The evidence for the hygiene hypothesis

Children who grow up on farms have lower rates of allergies. (John Moore/Getty Images)

In the decades since, all sorts of epidemiological evidence has been collected that supports Strachan’s idea. He initially found that in Britain, children who grew up in larger families also had lower chances of developing asthma and hay fever , presumably because they were exposed to more bacteria from their siblings.

Other doctors have found that, on the whole, people in wealthy, more heavily sanitized nations have much higher rates of asthma and allergies than those in the developing world. This could be a function of natural variations among the populations, but more recently, doctors have found that people who move from a developing country to a wealthier one have a higher chance of developing these diseases than people who stay in their country of origin.

kids who grow up on farms or have pets have lower rates of allergies and asthma

Even within a developing country like Ghana, wealthy urban children have higher rates of these autoimmune diseases than poorer or rural children. In the wealthy world, adults who clean their houses with antibacterial sprays have higher asthma rates, and people who are more often exposed to triclosan (the active ingredient in antibacterial soap) have higher rates of allergies and hay fever . Kids who grow up on farms or have pets, meanwhile, have lower rates of allergies and asthma .

These are all correlations — not causations — but they suggest that something about the relatively clean, modern urban environment makes these autoimmune diseases more likely to develop. And the handful of controlled studies conducted on the topic have provided further support — such as one, conducted recently in Uganda , in which babies born to mothers who were given drugs to treat parasitic worm infections during pregnancy ended up having higher rates of eczema and asthma.

Controlled studies with animals have also provided compelling evidence for the idea. “In experimental studies with germ-free mice raised in a sterile environment, researchers have found they’re extremely prone to developing colitis and asthma, among many other problems,” von Mutius says. But interestingly, if during childhood, these ultra-sanitized mice are inoculated with the stomach bacteria present in normal mice, they no longer have an increased autoimmune disease risk . Somehow, not being exposed to bacteria during childhood seems to increase the risk of autoimmune diseases, for both mice and humans.

How bacteria might prevent disease

A human T cell, shown under a microscope. (NAID)

Increased evidence for the hygiene hypothesis has come as scientists in general have awakened to the importance of "good" bacteria in our bodies in general. The particular species living inside your body — collectively called the microbiome — may be involved in preventing obesity , diabetes , and perhaps even depression .

Scientists have proposed several different mechanisms for how limited exposure to bacteria could lead autoimmune disorders to develop in particular. The most likely one, at the moment, involves specialized cells that are part of your immune system called T cells .

without being exposed to enough bacteria, our immune systems may not be able to learn to properly recognize harmful invaders

As part of the same mouse experiments, scientists found that the bacteria-free mice had exceptionally high numbers of these cells present in their stomachs and lungs. Normally, T cells serve a number of roles in the immune system — among other things, they recognize and eliminate harmful viruses and bacteria — but in some cases, certain types of T cells have previously been found to play a role in the development of colitis and asthma in mice . That seemed to be the case in the disease-stricken, ultra-clean mice as well — because when the scientists dosed them with a chemical that deactivated these T cells, they no longer developed the autoimmune diseases at such high rates.

If the same mechanism exists in humans, it would help explain all these epidemiological findings about autoimmune diseases — and strongly support the hygiene hypothesis.

But why would abnormal T cell behavior occur in the absence of bacteria? One theory, called the "Old Friends" hypothesis , is that our immune systems as a whole evolved in the presence of bacteria, viruses, and small animals that naturally inhabit our bodies .

We still don’t fully understand how the immune system develops as we grow up, but the idea is that this exposure is actually necessary for it to develop properly. Without being regularly exposed to bacteria, it can’t learn to properly recognize the few harmful invaders that need to be eliminated. As a result, autoimmune diseases — in which the immune system erroneously turns on our own bodies, effectively attacking ourselves — become more common.

But there’s still some disagreement among scientists

(Media for Medical/UIG via Getty Images)

At the moment, the hygiene hypothesis is still a hypothesis: a working theory, subject to change.

One major caveat is that no scientists believe it can account for all cases of allergies and asthma. Autoimmune disorders have a clear genetic component, so interactions between a person’s environment and genes contribute to rates of autoimmune diseases.

no scientists believe this can account for all cases of allergies and asthma

Additionally, there are some who believe that the theory can explain increases in some sorts of allergies, but not asthma , partly because asthma rates in the wealthy world didn't begin increasing until the 1980s, decades after present-day levels of sanitation were largely established. It's possible that there are varieties of asthma triggered by allergic reactions, and other types that aren't — and are actually exacerbated by exposure to dust and other less sanitary conditions.

Even regarding allergies, there are all sorts of other epidemiological questions that can’t be answered by the hygiene hypothesis — such as why, in some European cities, the children of migrants from other countries have lower rates of allergies than other children, even though they basically live in the same conditions. Clearly, we’re still in the early stages of understanding the development of the immune system, and don’t fully know how bacteria exposure affects it.

Perhaps most importantly, all scientists agree that basic sanitary practices have brought us enormous benefits: they’ve saved millions of lives by cutting down on all sorts of infectious diseases, and are probably the most important health advances we’ve made as a species so far.

So the key is using research to figure out the proper balance of sanitation and bacteria exposure, in order to limit the spread of infectious diseases without prompting increases in autoimmune disorders.

So what does this mean for you?

(Getty Images)

None of this means that you should stop cleaning your house or washing yourself, or begin drinking potentially sewage-contaminated water.

none of this means you should stop cleaning your house or washing yourself

For one, most of these findings involve bacteria exposure during childhood — not for adults. Additionally, most of the reduction in bacteria exposure we have in modern society comes from broader trends (like antibiotic overuse and sewage treatment plants) rather than personal choices.

So, at the moment, the practical applications of this research on a personal level are relatively limited. It might make you think twice before having your kid use antibiotic soap (which you really shouldn't be using anyway ). More importantly, it provides some evidence that vaginal births and breastfeeding are important for the development of a healthy microbiome in infants.

But what’s more important is how the hygiene hypothesis will guide doctors’ thinking about the growth of autoimmune diseases. In the future, if scientists are able to better understand the mechanisms of the hygiene hypothesis at the cellular level, we might be able to figure out how to balance basic sanitation with bacteria exposure — and the right kind of exposure to prevent allergies, inflammatory bowel diseases, and asthma from developing.

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A geneticist says any new parent should 'roll their child on floor of the New York subway' — here's why

A team of geneticists made headlines a few months ago after its mission to document all the bacteria on the New York City subway turned up nearly 600 different species of microbes crawling around on all those greasy rails.

They found some icky stuff, including the bacteria that give people food poisoning, and the bugs that can cause meningitis.

But before opting for an Uber, keep this in mind: Almost all of the germs they found were completely harmless.

In fact, those creepy-crawlies might actually be good for people.

According to an idea called the hygiene hypothesis , exposure to germs and certain infections — especially at a young age — actually helps prime the immune system so it can defeat these microbes more easily in the future.

Some research has suggested that the idea could partially explain why children who grow up around animals and in rural areas appear to develop conditions like asthma less often than children who don't. More studies, however, are necessary.

And even for people other than young children, the hygiene hypothesis makes intuitive sense: After all, literally every surface in the world is covered in bacteria. The idea that things can be "perfectly clean" is a myth — humans need bacteria to live.

"We tend to think of our homes and personal environments as these pristine places, and public ones as dirty and infested with bacteria," Chris Mason, a Weill Cornell Medical College geneticist and the author of the subway-pathogen study, recently said at a public event in New York. "But you should really think of yourself as a rabbit who gets to hop between two forests."

That's why Mason isn't afraid to let his own young daughter ride the subway or play in the dirt.

"I would advise any new parent to roll their child on the floor of the New York subway," said Mason.

Like the surfaces people touch and the ground they walk on, the human body is already teeming with thousands of different species of bacteria, from the Lactobacillus acidophilus lining digestive tracts to the Propionibacterium acnes populating the skin on faces and arms. On average, about three pounds of our body weight is accounted for by bacteria alone.

So the idea that a little more exposure couldn't hurt makes sense. Perhaps everyone should be a little less germaphobic.

Watch: Scientists just discovered 11,000-foot ice mountains, geysers, and volcanoes on Pluto

Main content

Is Being Too Clean Bad for Your Health?

From taking a shower to brushing your teeth to washing your hands, you practice good personal hygiene on the daily. And it’s not just because you like the way your new shampoo smells, either. You know these habits keep you clean and, in some cases, can even help prevent you from getting sick.

But after all that lathering, rinsing and scrubbing, can you actually be too clean for your own good?

That’s what supporters of the so-called hygiene hypothesis think, saying that the rising rates of allergies, asthma and other autoimmune disorders in children is linked to our increasingly hygienic surroundings. And while statistics appear to back this up, experts in the fields of immunology and infectious disease say, not so fast.

“To say that being clean means you’re at a higher risk of allergies or asthma is not quite right,” agrees Dr. John Lynch , an associate microbiology professor at the University of Washington School of Medicine and medical director of Harborview Medical Center’s Infection Control, Antibiotic Stewardship and Employee Health programs.

The problem, he says, is that the hygiene hypothesis doesn’t tell the full story.

What is the hygiene hypothesis?

Largely popularized by British epidemiologist David Strachan in 1989, the hygiene hypothesis theorizes that because modern parents are able to clean their children and households more effectively, kids these days just aren’t exposed to the same level of germs as previous generations.

That excessively sterile upbringing — hand sanitizer, anyone? — means children’s immune systems aren’t able to develop properly and, as a result, malfunction.

When you look at the statistics, they seem to support this idea. In developed countries, the number of kids who have asthma and allergies has been going up.

Washington state has some of the highest incidences of asthma in the nation, and it’s only increasing. More than 600,000 Washingtonians have asthma, and nearly 120,000 of them are children.

Research from the Centers for Disease Control and Prevention shows that the same trend applies to kids who have food allergies. Now 1 in 13 children in the United States has a food allergy, a 50% increase between 1997 and 2011. To put it in perspective, that means in every American classroom, there are two kids who may have a food-related allergic reaction.

Is the hygiene hypothesis true?

Don’t toss out your hand soap or quit bathing your kids just yet. Remember, while data appears to back up the hygiene hypothesis, it’s not a complete picture.

“There was no randomized control study to determine the hygiene hypothesis,” Lynch explains. “It ends up being observations of populations, biased by our ability to detect diseases. You have less likelihood of being diagnosed with asthma or even diabetes in a developing country versus a developed country.”

What Lynch means is that as the field of medicine has advanced in recent decades, so has our ability to detect and diagnose conditions like the aforementioned food allergies and asthma. And the reason why much of the evidence to support the hygiene hypothesis comes from industrialized countries is because these nations have greater medical infrastructure and resources to detect autoimmune dysfunctions than the developing world.

So while the number of children with asthma and food allergies is higher than in decades past, there’s no way to know if that’s because more kids actually have those conditions or if it’s because doctors are more able to recognize and diagnose those conditions.

Another problem with the hygiene hypothesis, Lynch notes, is that while getting exposed to some germs does help build up your immune systems, other types of bacteria and viruses can actually cause asthma or serious diseases.

That’s why researchers and medical professionals in Lynch’s field of infectious disease and immunology cringe at the name “hygiene hypothesis,” he says. It implies that good personal hygiene is related to higher rates of disease when, in fact, it’s the opposite.

Think about it this way: If the hygiene hypothesis is really accurate and being overly clean makes our immune systems malfunction, children who don’t wash their hands, are exposed to pathogens on a regular basis and live in unclean conditions would be the healthiest.

“Unfortunately, we know that people who live in places that lack access to hygiene die more frequently,” Lynch says.

How do you build up a child’s immune system?

It’s not that the hygiene hypothesis gets it all wrong. Children do need to be exposed to certain microorganisms in order to influence the right immune response and develop a robust immune system. And having a too-clean environment can hinder that in some ways.

“We don’t need to sterilize things with antibacterial products or create an incredibly hygienic environment,” Lynch says. “You don’t want to put any extra chemicals or agents in anything because that’s how you create antibiotic-resistant bacteria.”

In fact, your body is full of trillions of bacteria, fungi and viruses — an entire community called your microbiota — which are critical to your immune response and overall health.

Now here’s where glimmers of the hygiene hypothesis come in: Children develop a healthy microbiota by acquiring bacteria in a variety of ways, from vaginal birth and breastfeeding to getting kissed by their parents and sticking their fingers in their mouths as babies.

“That’s all normal,” Lynch says. “We don’t want women washing their breasts before breastfeeding or parents washing their lips before kissing their children.”

What also matters for immune development, though, is what you’re exposed to and how that affects your body. Getting a common cold virus is a totally normal part of childhood. But being exposed to an antibiotic-resistant superbug is a much more serious issue.

“When you’re talking about the hygiene hypothesis, the point of contention is that the focus should be less about hygiene and more about access to the right microbiota,” Lynch explains.

What’s the takeaway from the hygiene hypothesis controversy?

So while the hygiene hypothesis isn’t totally correct, going in the opposite direction to an overly sterilized childhood isn’t exactly healthy either. It can feel like the balance between exposing children to good bacteria and keeping them safe from the bad stuff is pretty much out of your control.

Just try to keep everything in perspective, Lynch says. Use common sense — and maybe go easy on the hand sanitizer.

“I like to think of it like this: Hand washing is important if you’re around someone who’s sick or if your kid is rolling around on the floor at a restaurant, but maybe not so much if they’re just playing outside at the park,” he says.

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the hygiene hypothesis article

The Hygiene Hypothesis

Medical Author: Charles P. Davis, MD, PhD Medical Editor: Melissa Conrad Stöppler, MD

The "Hygiene Hypothesis" is a theory that suggests a young child's environment can be "too clean" to effectively stimulate or challenge the child's immune system to respond to various threats during the time a child's immune system is maturing. As a fetus, the immune system is thought to be repressed to avoid rejecting maternal tissue, but at birth, it must start to recognize antigens that may be linked to harmful infections. If the environment is "too clean," the hypothesis suggests that the immune system will not mature properly, and may not react appropriately when the child's immune system encounters germs ( viruses , bacteria, fungi, and parasites) or other environmental triggers ( pollen , animal dander, fungal spores) later in life. The hypothesis suggests that the lack of immune system challenge results in many people developing immune-related health problems such as asthma .

Although the term "Hygiene Hypothesis" was proposed in the late 1980's, many investigators trace its origins to earlier experiments with animals, mainly mice and rats born and raised in "germ-free" or sterile environments. When experimentally exposed to low doses of an infectious agent that would not harm normally raised rodents, these germ-free adolescent and young adult animals became infected quickly and often died. When examined, the infected animals showed a slow or blunted immune response in these situations. If they were raised to adolescence or adulthood as germ-free animals and then were slowly introduced to bacteria found in their normal gastrointestinal tracts, the rodent's immune response, when exposed to the same pathogen, was much better and the animals usually survived the infection.

The key to understanding how the hygiene hypothesis might explain the high level of asthma in developed nations (and perhaps a number of other diseases such as Crohn's disease, ulcerative colitis , or multiple sclerosis) is knowledge of how the immune system develops, matures, and self-regulates. Although the details of the development and function of the immune system can fill books, a very brief summation is as follows:

Stimulation of the immune system causes a number of immune cell types to proliferate (for example, T cells, B cells, macrophages, eosinophils, killer cells), some of which attack infectious agents directly, other produce substances (for example, antibodies and cytokines) that cause or potentiate immune attacks.
The hygiene hypothesis suggests that delays in exposure to normal bacteria in the body as well as disease-causing agents make a weaker immune response, and that in turn, produces a weaker ability of the immune system to recognize and respond to suppress the inflammatory response when it is challenged.
Researchers suggest that bacterial and parasitic organisms, when exposed to a maturing immune system, cause the continuing development to proceed normally. Consequently, in a "too clean environment," infants and young children may not have their immune systems challenged appropriately, and, according to the hygiene hypothesis, go on to develop problems such as asthma and other immune-related conditions.

Proving the hygiene hypothesis is difficult because of the complexity of the developing immune system, the difficulty in designing ethical studies in infants and young children, and getting control and experimental groups of children who have parents that would allow them to be involved in such studies. Like many hypotheses, aspects or parts of this hypothesis still can be examined with the scientific method. Such work is being done with the hygiene hypothesis. For example, the development of probiotics , the oral introduction of "live microorganisms" to the intestine, is related to this hypothesis. More closely related is the development and study of the use of parasite eggs to modulate the immune response in order to treat inflammatory diseases such as Crohn's disease by modifying the immune response.

Most proponents of the hygiene hypothesis do not suggest that parents expose infants and children to infectious organisms to stimulate their immune response. They do suggest, however, that infants and children may be too protected from other children and the environment so that they fail to develop a normal immune system. This protection or isolation (for example, sterile foods, constant cleaning of the infant and child, social isolation from other children, no outdoor playing) may make children prone to develop immune-related diseases.

Although other investigators suggest increases in asthma and other immune-related diseases are due to other factors (for example, pollution, smoking [ secondhand smoke in children], toxin ingestion, and others), each is still a hypothesis until proven by the data gathered and examined by scientific methodology. Unfortunately, this takes time, effort and research money so the clues and eventual answers to the hypothesis will not come easily. Perhaps future data will definitively show that humans can be "too clean."

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The hygiene theory: fact or fiction?

Affiliation.

1 Division of Community Health Sciences: GP Section, University of Edinburgh, UK. [email protected]
PMID: 15167035
DOI: 10.1097/01.moo.0000122311.13359.30

Purpose of review: The "hygiene hypothesis" offers a potentially credible and parsimonious explanation for the increasing prevalence of allergy noted in many westernized populations. The authors review recent evidence both for and against this hypothesis.

Recent findings: A strong body of epidemiologic evidence indicates that the original observations, namely of a birth order effect and increased risk of atopic disorders in those born into small, affluent households, are robust findings. Improved hygiene is believed to mediate its effect through decreased exposure to infectious agents in early life, and recent evidence has focused attention on the importance of the gastrointestinal microbial environment. In particular, infection with hepatitis A, Helicobacter pylori, and toxoplasma in those living in temperate climates, and geoheminths in those living in endemic areas, have been shown to be associated with reduced risk of atopic manifestations. It is postulated that these infections exert their effect through critically altering T-helper (Th)1/Th2 regulation, which is supported by the examination of the cytokine profiles of cord mononuclear cells when exposed to gastrointestinal flora and, furthermore, emerging evidence on the benefits of probiotics on symptoms of atopic dermatitis. Attempts to identify an inverse relation between Th1- and Th2-mediated disorders (as might be predicted by the Th1/Th2 paradigm) have, however, yielded conflicting results, raising the possibility that this model may be something of an oversimplification.

Summary: The hygiene hypothesis remains a credible but nonspecific explanation for observed variations over time, place and persons at risk for developing atopic allergic disorders. More prospective studies are needed to unravel which infectious agents exert a protective effect and the time period of importance for sensitization. The clinical implications of these advances in our understanding of the etiology of atopic allergic disorders are currently limited.

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Clin Exp Immunol
v.160(1); 2010 Apr

The ‘hygiene hypothesis’ for autoimmune and allergic diseases: an update

According to the ‘hygiene hypothesis’, the decreasing incidence of infections in western countries and more recently in developing countries is at the origin of the increasing incidence of both autoimmune and allergic diseases. The hygiene hypothesis is based upon epidemiological data, particularly migration studies, showing that subjects migrating from a low-incidence to a high-incidence country acquire the immune disorders with a high incidence at the first generation. However, these data and others showing a correlation between high disease incidence and high socio-economic level do not prove a causal link between infections and immune disorders. Proof of principle of the hygiene hypothesis is brought by animal models and to a lesser degree by intervention trials in humans. Underlying mechanisms are multiple and complex. They include decreased consumption of homeostatic factors and immunoregulation, involving various regulatory T cell subsets and Toll-like receptor stimulation. These mechanisms could originate, to some extent, from changes in microbiota caused by changes in lifestyle, particularly in inflammatory bowel diseases. Taken together, these data open new therapeutic perspectives in the prevention of autoimmune and allergic diseases.

Introduction

Changes of lifestyle in industrialized countries have led to a decrease of the infectious burden and are associated with the rise of allergic and autoimmune diseases, according to the ‘hygiene hypothesis’. The hypothesis was first proposed by Strachan, who observed an inverse correlation between hay fever and the number of older siblings when following more than 17 000 British children born in 1958 [ 1 ]. The original contribution of our group to the field was to propose for the first time that it was possible to extend the hypothesis from the field of allergy, where it was formulated, to that of autoimmune diseases such as type 1 diabetes (T1D) or multiple sclerosis (MS) [ 2 ]. The leading idea is that some infectious agents – notably those that co-evolved with us – are able to protect against a large spectrum of immune-related disorders. This review summarizes in a critical fashion recent epidemiological and immunological data as well as clinical studies that corroborate the hygiene hypothesis.

The strongest evidence for a causal relationship between the decline of infections and the increase in immunological disorders originates from animal models and a number of promising clinical studies, suggesting the beneficial effect of infectious agents or their composites on immunological diseases.

In this review, we shall attempt to evaluate the arguments in favour of the hygiene hypothesis with particular interest on the underlying mechanisms.

Evolving epidemiology of allergic and autoimmune diseases

The rising incidence of atopic and autoimmune diseases.

In 1998, about one in five children in industrialized countries suffered from allergic diseases such as asthma, allergic rhinitis or atopic dermatitis [ 3 ]. This proportion has tended to increase over the last 10 years, asthma becoming an ‘epidemic’ phenomenon [ 4 ]. The increasing prevalence of asthma is important in developed countries (more than 15% in United Kingdom, New Zealand and Australia) but also in developing countries, as illustrated by a prevalence greater than 10% in Peru, Costa Rica and Brazil. In Africa, South Africa is the country with the highest incidence of asthma (8%) [ 5 ]. Unfortunately, data from most other African countries are unavailable [ 6 ]. The prevalence of atopic dermatitis has doubled or tripled in industrialized countries during the past three decades, affecting 15–30% of children and 2–10% of adults [ 7 ]. In parallel, there is also an increase in the prevalence of autoimmune diseases such as T1D, which now occurs earlier in life than in the past, becoming a serious public health problem in some European countries, especially Finland, where an increasing number of cases in children of 0–4 years of age has been reported [ 8 ]. The incidence of inflammatory bowel diseases (IBD), such as Crohn's disease or ulcerative colitis [ 2 ] and primary biliary cirrhosis [ 9 ] is also rising. Part of the increased incidence of these diseases may be attributed to better diagnosis or improved access to medical facilities in economically developed countries. However, this cannot explain the marked increase in immunological disorder prevalence that has occurred over such a short period of time in those countries, particularly for diseases which can be diagnosed easily, such as T1D or MS [ 10 – 12 ].

The decreasing incidence of infectious diseases

Public health measures were taken after the industrial revolution by western countries to limit the spread of infections. These measures comprised decontamination of the water supply, pasteurization and sterilization of milk and other food products, respect of the cold chain procedure, vaccination against common childhood infections and the wide use of antibiotics. The decline is particularly clear for hepatitis A (HAV), childhood diarrhoea and perhaps even more spectacular for parasitic diseases such as filariasis, onchocercosis, schistosomiasis or other soil-transmitted helminthiasis [ 13 ]. In countries where good health standards do not exist, people are chronically infected by those various pathogens. In those countries, the prevalence of allergic diseases remains low. Interestingly, several countries that have eradicated those common infections see the emergence of allergic and autoimmune diseases.

Uneven distribution

The geographical distribution of allergic and autoimmune diseases is a mirror image of the geographical distribution of various infectious diseases, including HAV, gastrointestinal infections and parasitic infections. There is an overall North–South gradient for immune disorders in North America [ 14 ], Europe [ 2 ] and also in China [ 15 ] with intriguing exceptions such as asthma in South America or T1D and MS in Sardinia. There is also a West–East gradient in Europe: the incidence of T1D in Bulgaria or Romania is lower compared to western Europe, but is increasing fast [ 16 ]. This gradient cannot be fully explained by genetic differences. Indeed, the incidence of diabetes is sixfold higher in Finland compared to the adjacent Karelian republic of Russia, although the genetic background is the same [ 17 ].

Additionally, migration studies have shown that offspring of immigrants coming from a country with a low incidence acquire the same incidence as the host country, as rapidly as the first generation for T1D [ 18 ] and MS [ 19 , 20 ]. This is well illustrated by the increasing frequency of diabetes in families of immigrants from Pakistan to the United Kingdom [ 21 ] or the increasing risk of MS in Asian immigrants moving to the United States [ 22 ]. The prevalence of systemic lupus erythematosus (SLE) is also much higher in African Americans compared to West Africans [ 23 ].

These data do not exclude the importance of genetic factors for those immunological disorders, as assessed by the high concordance of asthma, T1D or IBD in monozygotic twins: for example, the concordance rate for atopic dermatitis among monozygotic twins is high (77%) compared to dizygotic twins (15%) [ 7 ]. The difference in some genetic factors according to ethnicity [human leucocyte antigen (HLA) gene difference between Caucasian and Asian, for example] is well documented, but probably plays a minor role in geographical distribution in view of migrant data.

Search for risk factors at the origin of the increase of immunological disorders

Several factors, such as socio-economic indices, may explain the difference in the prevalence of immunological disorders according to time and geographical distribution. In fact, there is a positive correlation between gross national product and incidence of asthma, T1D and MS in Europe [ 2 ]. This is true at the country level, but also at that of smaller regions, such as Northern Ireland, where the low incidence of T1D is correlated with low average socio-economic level, as evaluated by conventional indices [ 24 ]. Similar results have been obtained in the province of Manitoba in Canada for Crohn's disease [ 25 ]. This correlation has even been demonstrated at the individual level for atopic dermatitis, as family income is correlated directly with the incidence of the disease [ 26 ]. However, this does not pinpoint which factor within the socio-economic indices is directly responsible for the immunological disorder. Several epidemiological studies have indicated a positive correlation between sanitary conditions and T1D [ 24 ] or MS [ 27 ], suggesting a possible role of infections. Other factors are often incriminated, such as air pollution for asthma [ 28 ], but their role has not been demonstrated convincingly. For example, it has been shown that in East Germany before the fall of the Berlin Wall, where the air pollution was greater, the incidence of asthma was lower than in West Germany [ 29 ].

Vitamin D production is linked to sun exposure, and has been shown recently to have immunomodulatory effects [ 30 ]. However, this does not explain the West–East gradient of T1D in Europe, or the huge difference between Finland and its neighbouring Karelian region, where people have the same sun exposure level [ 31 ].

Epidemiological data indicating a direct link between the decreasing level of infectious burden and the rising incidence of immunological disorders

Several epidemiological studies have investigated the protective effect of infectious agents in allergic and autoimmune diseases. The presence of one or more older siblings protects against development of hay fever and asthma [ 1 ], of MS [ 32 ] and also of T1D [ 33 ], as does attendance at day care during the first 6 months of life in the case of atopic dermatitis and asthma [ 34 ].

Interestingly, exposure to farming and cowsheds early in life prevents atopic diseases, especially if the mother is exposed during pregnancy [ 35 , 36 ]. It has also been shown that prolonged exposure to high levels of endotoxin during the first year of life protects from asthma and atopy [ 37 ]. However, these data have been contradicted by other studies showing an increased prevalence of asthma correlated with higher levels of endotoxins in urban housing [ 38 , 39 ]. The level of endotoxins is higher in farms as compared to cities, and subjects are in contact with a greater variety of microbial compounds in farms, which could explain this discrepancy.

Do helminth parasites protect against atopy? Epidemiological data of cross-sectional studies revealed that Schistosoma infections have a strong protective effect against atopy, as reviewed recently [ 40 ]. Hookworms such as Necator americanus also seem to protect from asthma. In contrast, Ascaris lumbricoides and Trichuris trichiura have no significant effect on disease. Parasitic infections have been almost eradicated in European countries since the Second World War, concomitant with the increase of atopy and allergy. This trend can explain part of the epidemiological difference between Europe and Africa, but cannot explain readily the intra-European North–South gradient.

Proof of principle of the causal relationship between decline of infectious diseases and increase of immunological disorders

We have seen that there is a strong correlation between changes in lifestyle and modifications of the incidence of allergic or autoimmune diseases, but this does not prove a causal relationship between these two observations. This is a crucial question, as many factors unrelated to infections are a consequence of lifestyle, such as food habits, quality of medical care or dinner time gradient from North to South Europe. The answer to this question comes from animal models of autoimmune and allergic diseases and, to a lesser degree, from clinical intervention studies.

Animal models

The incidence of spontaneous T1D is directly correlated with the sanitary conditions of the animal facilities, for both the non-obese diabetic (NOD) mouse [ 2 ] and the bio-breeding diabetes-prone (BB-DP) rat [ 41 ]: the lower the infectious burden, the higher the disease incidence. Diabetes has a very low incidence and may even be absent in NOD mice bred in ‘conventional’ facilities, whereas the incidence is close to 100% in female mice bred in specific pathogen-free (SPF) conditions. Conversely, infection of NOD mice with a wide variety of bacteria, virus and parasites protects completely (‘clean’ NOD mice) from diabetes [ 2 ]. Similarly, mycobacteria (e.g. complete Freund's adjuvant) prevent induction of experimental autoimmune encephalomyelitis [ 42 ] and ovalbumin-induced allergic asthma [ 43 ]. Data obtained in our laboratory show that living pathogens are not required, as bacterial extracts are sufficient to afford protection [ 44 ].

Increased atopy after anti-parasitic treatments

It has been shown that helminth eradication increases atopic skin sensitization in Venezuela [ 45 ], in Gabon [ 46 ] and in Vietnam [ 40 ]. However, in a small study of 89 Venezuelan adults and children with asthma there was a clinical improvement, and specific immunoglobulin E (IgE) levels decreased after anti-helminthic treatment [ 47 ], while a similar deworming treatment showed no effect in Ecuador [ 48 ]. It is difficult to explain these contradictory data, which may relate to the complexity of asthma pathophysiology. In the same vein, one might also mention the increased atopy observed after vaccination with Streptococcus pneumoniae in South Africa [ 49 ].

Prevention of allergic and autoimmune diseases by infections

In a prospective study in Argentina, 12 patients with MS with high peripheral blood eosinophilia were followed. These patients presented parasitic infections and showed a lower number of MS exacerbations, increased interleukin (IL)-10 and transforming growth factor (TGF)-β secretion by peripheral blood mononuclear cells (PBMC) [ 50 ].

Similarly, deliberate administration of ova from the swine-derived parasite Trichuris suis , every 3 weeks for 6 months to 29 patients with active Crohn's disease, improved symptoms in 21 of 29 patients (72%) with no adverse events [ 51 ]. T. suis ova were also given to patients with active ulcerative colitis, with significant improvement (43% improvement versus 17% for placebo) [ 52 ].

Another helminth, Necator americanus , has also been used in Crohn's disease, patients being inoculated subcutaneously with infective larvae. There was a slight improvement of symptoms, but the disease reactivated when immunosuppressive drugs were reduced [ 53 ].

Probiotics are non-pathogenic microorganisms that are assumed to exert a positive influence on host health and physiology [ 54 ]. Encouraging results were first shown in a double-blind randomized placebo-controlled trial in Finland, where Lactobacillus GG taken daily by expectant mothers for 2–4 weeks before delivery and postnatally for 6 months could decrease significantly the incidence of atopic dermatitis [ 55 ]. Perinatal protection lasted up to 7 years [ 56 ]. Another trial showed improvement of atopic dermatitis using other strains of probiotics [ 57 ]. However, a German group using the same protocol did not find any protective effect after 2 years [ 58 ]. Additionally, a recent study of 445 pregnant women in Finland who were treated with the same protocol as the initial Finnish study, but with freeze-dried Lactobacillus GG , failed to show any significant effect on eczema, allergic rhinitis or asthma 5 years after treatment. The only difference observed was a decreased IgE-associated allergic disease in caesarean-delivered children [ 59 ].

In T1D, only experimental data are available. The protective effect of a probiotic [ 60 ] and a bacterial extract [ 44 ] was reported on the onset of diabetes in NOD mice. A pilot study in humans, the PRODIA study (probiotics for the prevention of beta cell autoimmunity in children at genetic risk of type 1 diabetes), was begun in 2003 in Finland in children carrying genes associated with disease predisposition [ 61 ].

The case of probiotics in IBD is more complex because of the possible local anti-inflammatory effect, which could explain the relief of symptoms without changes in disease progression, as implicated in the hygiene hypothesis. Following a number of uncontrolled studies in a small cohort of 14 paediatric patients with newly diagnosed ulcerative colitis, probiotic treatment induced a significant rate of remission compared to the control group (93% versus 36%) and a lower relapse rate [ 62 ].

In brief, there are data suggesting that probiotics may have a favourable role in immune disorders, but the case is far from proven and requires further investigation. Additionally, although side effects are very low they might not be non-existent, as shown in a set of patients with acute pancreatitis [ 63 ]. Thus, probiotics should not be considered as totally harmless, particularly in the immunodeficient host, and more safety studies are needed. As mentioned by Sharp et al ., ‘probiotics may have unpredictable behaviour like all microorganisms, such as unanticipated gene expression in non-native host environment, or acquired mutations occurring spontaneously via bacterial DNA-transfer mechanisms’.

Is there a role for microbiota changes in the hygiene hypothesis?

The human gut is the natural niche for more than 10 14 bacteria of more than 1000 different species [ 64 ]. Immediately after birth, the human gut is colonized with different strains of bacteria. This commensal microbiota is important in shaping the immune system, for other basic physiological functions [ 65 ] as well as for the integrity of the intestinal barrier [ 66 ]. Interestingly, the intestinal flora was different in a small group of allergic Estonian and Swedish children compared to the control group, with a higher count of aerobic bacteria such as coliforms and Staphylocccus aureus and a decreased proportion of Lactobacilli , or anaerobes such as Bifidobacterium or Bacteroides [ 67 , 68 ]. However, this difference was not seen in a larger birth cohort study comparing three European baby populations [ 69 ]. Additionally, this study showed a slower acquisition of typical faecal bacteria such as Escherichia coli , especially in children delivered by caesarian section or children without siblings. It should be noted that all these studies were based on the analysis of culturable bacteria, and only atopic dermatitis and skin prick test were evaluated.

In autoimmune diseases the microbiota also seems to modulate the immune response. In NOD mice deficient for the myeloid differentiation primary response gene 88 (MyD88) signalling molecule it has been shown that microbiota protect mice from diabetes via a MyD88-independent pathway [ 70 ]. Using the metagenomic approach, it has been demonstrated that the biodiversity of the faecal microbiota of patients with Crohn's disease is diminished, especially for the Firmicutes phylum [ 71 , 72 ]. Faecalibacterium prautsnitzii is one of the Firmicutes that was particularly depleted, and it has been shown that this deficient commensal bacterium could improve IBD in a murine model of the disease [ 73 ]. This protective effect was also obtained with the supernatant of F. prautsnitzii culture, demonstrating the importance of one of the secreted molecules for its anti-inflammatory effect. Another bacterium, Bacteroides fragilis , has also been shown to protect animals from experimental colitis, and this protective effect was linked to a single microbial molecule, polysaccharide A [ 74 ]. As mentioned above, with regard to IBD these data must be interpreted with caution before extrapolating to other autoimmune disorders where the disease site is extra-intestinal. First, the respective anti-inflammatory and immunomodulatory effects of protective bacteria remain to be determined. Secondly, this protective effect should be discussed in the context of disease-promoting bacteria such as Helicobacter hepaticus .

In brief, there is an increasing amount of data showing that microbiota changes could contribute to the modulation of immune disorders but evidence is still slim, except in IBD. It is to be hoped that studies which provide a fair description of the molecular changes following intestinal infections will help in analysing the question further. The recent report by Fumagalli et al . is a good illustration of this new approach [ 75 ].

Mechanisms of the hygiene hypothesis

When considering the multitude of infectious agents that can induce protection from various immunological disorders, it is not surprising that more than one single mechanism has been found.

T helper type 1 (Th1)–Th2 deviation

Th1–Th2 deviation was the first major candidate mechanism for explaining the protective influence of infectious agents from immunological disorders. Th1 T cells produce inflammatory cytokines such as IL-2, interferon (IFN)-γ and tumour necrosis factor (TNF)-α that are operational in cell-mediated immunity (including autoimmune diabetes). In contrast, Th2 T cells that produce IL-4, IL-5, IL-6 and IL-13 contribute to IgE production and allergic responses. Given the reciprocal down-regulation of Th1 and Th2 cells, some authors suggested initially that in developed countries the lack of microbial burden in early childhood, which normally favours a strong Th1-biased immunity, redirects the immune response towards a Th2 phenotype and therefore predisposes the host to allergic disorders. The problem with such an explanation is that autoimmune diseases, which in most cases are Th1 cell-mediated, are protected by infections leading to a Th1 response and that atopy may be protected, as seen above, by parasites which induce a Th2 response. These observations fit with the concept of a common mechanism underlying infection-mediated protection against allergy and autoimmunity. Several hypotheses may explain these common mechanisms.

Antigenic competition /homeostasis

It has been known for several decades that two immune responses elicited by distinct antigens occurring simultaneously tend to inhibit each other. Numerous mechanisms were evoked to explain antigenic competition that might be pertinent to the hygiene hypothesis. The development of strong immune responses against antigens from infectious agents could inhibit responses to ‘weak’ antigens such as autoantigens and allergens. Among the mechanisms that explain antigenic competition, attention has been drawn recently to lymphocyte competition for cytokines, recognition for major histocompatibility complex (MHC)/self-peptide complexes and growth factors necessary to the differentiation and proliferation of B and T cells during immune responses within the frame of lymphocyte homeostasis. Similarly to red blood cell mass, which is restored to normal levels after a haemorrhage with the help of erythropoietin, CD4 and CD8 T lymphocytes are restored to normal levels after a lymphopenia. Homeostatic factors that play an equivalent role to that of erythropoietin have not been elucidated completely; however, cytokines such as IL-2, IL-7, and IL-15 are known to play a crucial role. Regulatory T cells that we discuss below may also be implicated in the mechanism of antigenic competition.

Immunoregulation

Another mechanism involves regulatory T cells which can suppress immune responses distinct from reponses against the antigen in question, here antigens expressed by infectious agents (a phenomenon called bystander suppression). The problem is complicated by the multiplicity of regulatory lymphocytes involving diverse cytokines that mediate their differentiation or their regulatory effects. The role of CD4 + CD25 + forkhead box P3 (FoxP3 + ) T cells has been suggested by transfer experiments performed in a murine parasite model [ 76 ]. The role of such cells is also suggested by the observation that CD28 –/– NOD mice devoid of CD4 + CD25 + FoxP3 + regulatory T cells (T regs ) lose their sensitivity to the protective effect of bacterial extract (our unpublished data). It has also been reported that in cord blood from newborns of mothers exposed to farming, CD25 + FoxP3 cells were up-regulated [ 77 ]. This observation should be interpreted with caution because of the uncertain specificity of these markers in man.

Other data suggest a role for IL-10-producing B cells [ 78 ], natural killer (NK) T cells [ 79 ] and more generally cytokines such as IL-10 [ 80 ] and TGF-β[ 81 ] whatever the cell type producing these cytokines. More work is needed in experimental models to delineate further the involvement of regulatory mechanisms in the protective effects of the various infections relevant to the hygiene hypothesis. It might emerge that different mechanisms are operational according to the protective infection.

Non-antigenic ligands

All the mechanisms mentioned previously are based on the notion that the hygiene effect is due to the decrease of immunological responses elicited against infectious agents. A number of experiments indicate that infectious agents can promote protection from allergic diseases through mechanisms independent of their constitutive antigens, leading to stimulation of non-antigen specific receptors. This concept is well illustrated by the example of Toll-like receptors (TLRs). Knowing the capacity of TLRs to stimulate cytokine production and immune responses, it might be predicted that TLR stimulation by infectious ligands should trigger or exacerbate allergic and autoimmune responses. This has indeed been demonstrated in some experimental models [ 82 , 83 ].

Surprisingly, and paradoxically, it has also been observed that TLR stimulation could prevent the onset of spontaneous autoimmune diseases such as T1D in NOD mice, an observation made for TLR-2, -3, -4, -7 and -9 [ 84 ] (and our unpublished data). In this model, treatment with TLR agonists before disease onset prevents disease progression completely. The mechanisms underlying such protections are still ill defined, but could involve production of immunoregulatory cytokines and the induction of regulatory T cells or NK T cells. Similar data have been observed in an ovalbumin-induced model of asthma [ 85 ].

Concerning HAV, it was shown initially that atopic diseases were less common in subjects that have been exposed to the virus [ 86 ]. It was difficult to say whether this association was due to a direct protective effect of HAV infection or explained only by the fact that HAV exposure is a matter of poor hygiene. Data obtained by Umetsu et al . have shown that HAV could influence T cells directly, notably Th2 cells that express the HAV receptor [ 87 ], a finding corroborated by the observation that atopy prevalence is associated with HAV receptor gene polymorphisms in anti-HAV antibody-positive subjects. In fact, recent data indicate that the HAV receptor, the TIM-1 protein (T cell, immunoglobulin domain and mucin domain), could play an important role in the severity of HAV and its putative effect on atopic diseases.

Gene–environment interactions

An interesting approach to identify mechanisms underlying allergic and autoimmune diseases consists in searching for associations between these diseases and polymorphisms of various genes, notably those coding for molecules involved in immune responses. It is interesting to note that such an association has been found for genes implicated in the control of infection. Among them, polymorphism in genes of the innate immune response such as CD14 , TLR2 , TLR4 , TLR6 or TLR10 , and intracellular receptors such as NOD1 and NOD 2 [also known as caspase-recruitment domain (CARD)4 and CARD15, respectively], appears to be important [ 88 , 89 ]. Mouse studies have shown that these gene–environment interactions explain a proportion of the phenotypic variance. One of those genes is CD14 , which is important in lipopolysaccharide (LPS)/TLR-4 signalling. Many association studies have highlighted the role of the CD14–159CT polymorphism and allergic inflammation [ 90 ].

Therapeutic strategies

The notions presented above open new, interesting, therapeutic perspectives for the prevention of allergic and autoimmune diseases. Of course, contaminating children or adults at high risk of developing these diseases by infectious agents cannot be envisioned, at a time when medical progress has allowed the reduction of major infectious diseases. It should be mentioned, however, that even if we do not believe that this is not the best strategy for the future, some groups have used living parasites such as T. suis in the prevention of IBD, as mentioned above, or living Lactobacilli in the prevention of atopic dermatitis. These approaches present the obvious limitation of insufficient standardization, and hazards linked to unpredictable disease course in subjects presenting an unknown immunodeficiency by contamination with xenogeneic virus in the case of swine-derived parasites.

Conversely, the use of bacterial extracts, already shown to be efficacious in a number of experimental models and in the clinic, such as OM-85 in T1D, should be envisioned seriously [ 44 ]. These extracts, which represent the mixture of a wide spectrum of chemically ill-defined components, are also submitted to the criticism of poor standardization. On the other hand, they are a better representation of the various components of bacteria known for their protective effects. The same comments apply to parasitic extracts, shown to be effective in T1D [ 91 ]. In the long-term future, one would like to use chemically defined components of protective infectious agents, such as TLR agonists, polysaccharide A or the active substance secreted by F. prautsnitzii . In any event, the use of bacterial extracts or chemically defined products will be confronted with the double problem of the timing of administration (sufficiently early in the natural history of the disease), and of safety. Indeed, any side effects are unacceptable in young subjects who are apparently healthy and whose risk of developing the disease in question is not demonstrated absolutely.

None of the authors has conflicts of interest to declare, or any relevant financial interest, in any company or institution that might benefit from this publication.

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What is the hygiene hypothesis?

by Bianca Nogrady

The idea that we need to be exposed to germs and bacteria in early childhood is the subject of much debate, but what is the hygiene hypothesis?

Published 28/03/2013

Emerging hypothesis

It's in the gut, healthy living and gut bacteria.

It sounds counter-intuitive, but not being exposed to viruses, bacteria and parasites in your early years could have a negative effect on your health, or at least that's what the hygiene hypothesis suggests.

The idea, which is subject to much debate, suggests our obsession with cleanliness and sterile surroundings is causing the increase in allergic and autoimmune diseases we've seen in recent decades.

Gastroenterologist Professor Timothy Florin says the term 'hygiene hypothesis' has been bandied around a lot, but has generally come to refer to the effect of children not being exposed to enough pathogens at an early age.

"The basis is that our immune system has evolved over evolutionary time as a defence against bacteria and viruses – bacteria and viruses have evolved over time with humans, rather like domestic dogs and pets, and they're used to seeing each other," says Florin, from the University of Queensland and Brisbane's Mater Hospital.

"So we're used to, in our growth as a population, seeing certain viruses at certain times and if you don't see them at that time then it's a bit like missing out on a maths lesson at a critical stage in infancy – you're missing certain building blocks."

The idea was first put forward in the 1980s by epidemiologist David Strachan, after he studied a cohort of more than 17,000 British children in an attempt to understand the gradual increase in incidence of hayfever in post-war Britain. During his research he noticed a striking pattern emerging.

The more older siblings a child had, the less likely he or she was to develop hay fever or eczema by age 23. He found it was by far and away the most important risk factor in determining whether a child developed the allergic condition.

Strachan concluded there must be some protective factor spread from older siblings to younger siblings.

"[These observations] could, however, be explained if allergic diseases were prevented by infection in early childhood, transmitted by unhygienic contact with older siblings, or acquired prenatally from a mother infected by contact with her older children," he wrote in the British Medical Journal, on the 18 November, 1989.

Since then, other studies have found links between various aspects of Western living standards and a range of allergic diseases – including eczema, asthma, and food allergy – or autoimmune conditions such as type 1 diabetes.

Research also suggests children born to families migrating to western countries also experience an increase in the incidence allergic disease. And it's been found certain factors – such as attending childcare or having a pet – can help to reduce the risk of allergic disease.

However, immunologist Professor Barbara Fazekas says the hygiene hypothesis has become something of a catch-all that is used to point the finger at a variety of 'modern evils'.

"Currently, the hygiene hypothesis seems to mean whatever you want it to mean – we're too clean, and we eat fast food and we do this and this," says Fazekas, Principal Research Fellow at the Centenary Institute of Cancer Medicine and Cell Biology, University of Sydney.

However she points to Strachan's research which showed differences in the risk of allergy between siblings of the same family. "None of those things that society is blamed for could possibly affect families in that way."

Fazekas, who describes herself as a 'hygiene hypothesis purist', believes the protective factor Strachan was reaching for has something to do with the gut microbiome – the microbiotic population of our gut – and its vital role in immune function.

"The gut has a huge surface area and most of our immune system is focused on the gut so that interaction is by far the biggest immune reaction that's going on in all of us all the time," Fazekas says.

Before birth, a baby's gut is sterile, but during birth and the first few days of life they begin to develop essential gut flora. Factors affecting the development of this gut flora include how a baby is delivered, early contact with parents and siblings, whether the baby or its mother are given antibiotics or other medications in hospital.

She believes as gut flora are established early in life and remain with us for life, they influence and educate the immune system everyday for our entire lives.

"I think that's much more likely to educate your cells all the time than something that happened in terms of a cough or a cold."

So how can improve our children's chances of developing healthy gut flora, while maintaining adequate hygiene?

Fazekas says it's not as simple as eating dirt.

"If we're talking about things that live in the human gut, most of the things that live in the human gut are adapted to live in the human gut and you get them from other humans, you don't get them from dirt," she says.

In her view, older siblings can help, as the original hygiene hypothesis paper illustrated, or exposure to other sources of diverse gut flora at an early age, such as child-care. Research also suggests having pets and spending time on farms could help.

But the hygiene hypothesis shouldn't be an excuse for poor hygiene, says Florin.

"It's important to be very hygienic in situations where there's some invasive bug going around, but within your own home where there's no epidemic bug going around, I don't think it's important to be hygienic at all."

Home hygiene quiz - ABC Health & Wellbeing
Does cleaning with antibacterial products reduce illness in the home - ABC Health & Wellbeing
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Clostridium difficile and the probiotic bomb - The Health Report
The hygiene hypothesis - Health Report - ABC Radio National
Vitamin D, the gut and food allergies - ABC Health & Wellbeing
What are the health benefits of probiotics? - ABC Health & Wellbeing

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What is the Hygiene Hypothesis?

A neighbor of mine says she believes in the hygiene hypothesis and that is why she doesn’t insist that her kids wash their hands before meals. She seems to be a good mother and her kids are great, but I wonder how their lack of hygiene will affect them. Your thoughts?

Andrew Weil, M.D. | November 26, 2013

Closeup shot of a father helping his baby girl wash her hands at a tap

Recent research from the U.K.’s University of Cambridge suggests that the hygiene hypothesis may also account for higher rates of Alzheimer’s disease in industrialized countries. The investigators looked at whether “pathogen prevalence” underlies levels of variation in Alzheimer’s rates across 192 countries. They found that countries with higher levels of sanitation had higher rates of Alzheimer’s, noting that countries such as the U.K. and France, where everyone has access to clean drinking water, have nine percent higher rates of the disease than Kenya, Cambodia and other countries where less than half the population has access to clean drinking water.

The hygiene hypothesis was first proposed by epidemiologist David Strachan in a 1989 article in the British Medical Journal . He had found that kids who grow up in large families are often healthier and less prone to allergies than kids with few siblings. Then, in the late 1990s German researcher Erika Von Mutius set out to study kids growing up in poor rural or polluted areas in Germany on the theory that they would have more allergies and asthma than kids who lived in more sanitary surroundings. She found the opposite to be true, and concluded that because the immune system of children growing up in hygienic conditions had not had much exposure to germs, they were more likely to react to harmless substances such as pollen or peanuts.

The human immune system has two types of defenses. The hygiene hypothesis holds that when one defensive system isn’t challenged by bacteria and other microbes early on – because of insufficient exposure – the other system becomes too powerful and tends to over-react to harmless substances.

Over the years there have been many studies on the hygiene hypothesis, but so far, nothing conclusive has been proved. One of the latest studies, from researchers at Boston’s Brigham and Women’s Hospital (BWH), found evidence that supports it, at least in mice. The team looked at the immune system of “germ-free” mice that do not harbor bacteria or any other microbes and compared them to regular mice living in a normal environment. They reported that the germ-free mice had exaggerated inflammation of the lungs and colon, resembling findings in human cases of asthma and colitis. They also found that exposing germ-free mice to microbes during their first weeks of life (but not when they became adults) led to normal immune responsiveness and long-lasting disease protection.

Richard Blumberg, M.D., co-senior author of the study was quoted in a BWH press release as saying that the studies “show the critical importance of proper immune conditioning by microbes during the earliest periods of life” and could enable scientists “to potentially identify the microbial factors important in determining protection from allergic and autoimmune diseases later in life.”

This is a fascinating area of research. Much more must be learned before the hygiene hypothesis can make the leap from intriguing idea to fact.

Andrew Weil, M.D.

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The Hygiene Hypothesis and Autoimmune Disorders

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The hygiene hypothesis is a hypothesis that suggests that the increased incidence of allergic and autoimmune disorders are linked to the tremendous changes in sanitation standards and practices that occurred in industrializing countries throughout the industrial revolution of the 19th and 20th centuries.

Throughout the last century, striking increases in the incidence of autoimmune diseases such as Type 1 diabetes mellitus and multiple sclerosis were evident.

The same holds good for allergic conditions such as atopic dermatitis, allergic rhinitis and asthma.

Although many factors are likely to be involved, including genetics and other triggering mechanisms, the rapidity of the changes appear to indicate the input of other changes, such as those seen in the environment.

This is supported by the finding that emigrants from a country with a low incidence of autoimmune disease to one with a high incidence of such acquire a high incidence of such conditions in the very first generation.

The associated changes in these countries that have witnessed drastic rises in the incidence of such diseases include the widespread use of antibiotics, milk pasteurization, vaccination against common childhood preventable diseases and a supply of almost sterile water.

In particular, the presence of certain microbes is thought to have a salutary effect on the robust functioning of the human immune system.

Throughout the industrial revolution, drastic changes in sanitation standards led to reduced or almost no exposure to these vital bacteria.

As a result, the function of the immune system was compromised, and the incidence of allergic and autoimmune disease began to rise.

Hygiene Hypothesis and “Old Friends” Hypothesis

Strachan first proposed the hygiene hypothesis in 1989, although some observations of the relationship between sanitation and autoimmune disorders had been noted previously.

An earlier observational study of more that 17,000 children in Britain in 1958 found an inverse relationship between allergic diseases such as hay fever, type 1 diabetes and asthma, and the number of older siblings.

Having attended a day care center early in life, within the first 6 months, protected against the development of asthma and atopy in children.

Another study in 1966 found a relationship between sanitation and the prevalence of multiple sclerosis. However, these findings were later extended to asthma and autoimmune diseases.

Relationship with Autoimmune Diseases

Diverse mechanisms have been proposed to explain the relationship between microorganisms and the prevention of autoimmune diseases.

The “old friends” microbes and the human immune system, including the distinctive antigens of the microbes, may work together in a reciprocal relationship. These antigens have been suggested to stimulate stronger immune responses, especially as compared to the autoantigens associated with autoimmune disorders.

Competition for cytokines, major histocompatibility complex (MHC) receptors and growth factors that are required for an immune response to occur is likely to be an important mechanism of protection against autoimmune disease.

The weak self-antigens and allergic antigens cannot compete successfully with the strong antigens which elicit immune responses in the case of other infections and parasitoses. Additionally, immunoregulatory interactions with the host toll-like receptors (TLRs) have been proposed as another mechanism.

Type 1 Diabetes

Type 1 diabetes, or insulin-dependent diabetes mellitus (IDDM), is becoming increasingly more prevalent worldwide, in both industrialized and developing countries.

This trend began in the 1970s in industrialized countries and continues today to become a public health problem in some countries, such as Finland. Additionally, younger children are now being seen to be affected by IDDM, including children under the age of 2 years, which was not before noted.

Multiple Sclerosis

In 1966, Leibowitz published an epidemiological study that observed a positive relationship between the prevalence of multiple sclerosis and levels of sanitation. It appeared that high levels of sanitation, such as those in the temperate areas of Israel, were associated with a higher risk of multiple sclerosis when compared to areas of lower sanitation, such as in tropical areas. This relationship has been further supported by other epidemiological studies designed to investigate the impact of the hygiene hypothesis on autoimmune diseases.

Inflammatory Bowel Diseases

The incidence of Crohn’s disease, ulcerative colitis and primary biliary cirrhosis is also increasing. This rise may be due in part to improved medical access and diagnostic techniques, but cannot be linked solely to these explanations. For this reason, an environmental link and the hygiene hypothesis is also thought to be involved.

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2841828/
http://www.nejm.org/doi/full/10.1056/NEJMra020100
http://link.springer.com/article/10.1007%2Fs12016-011-8285-8
http://perspectivesinmedicine.cshlp.org/content/2/2/a007799.full

Yolanda Smith

Yolanda graduated with a Bachelor of Pharmacy at the University of South Australia and has experience working in both Australia and Italy. She is passionate about how medicine, diet and lifestyle affect our health and enjoys helping people understand this. In her spare time she loves to explore the world and learn about new cultures and languages.

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Published: 05 August 2024

Personal hygiene practice and associated factors among elementary school students in Fiche Town, Oromia, Ethiopia

Getaneh Haile Minda 1 ,
Habiteyes Hailu Tola 1 ,
Abebe Feyissa Amhare 2 ,
Asefa Kebie 1 &
Tewodros Endale 1

BMC Infectious Diseases volume 24 , Article number: 781 ( 2024 ) Cite this article

Metrics details

Students in school are more likely to be sick from communicable diseases like diarrheal illnesses, acute respiratory infections, and other illnesses linked to poor personal hygiene. Poor hygiene practices are common among school children and put their health at risk, which in turn has several consequences. These include significant school absences, transmission of infectious diseases to other students, and missed workdays for parents and guardians. However, there is limited evidence on the level of personal hygiene practice and its associated factors among school students. Thus, this study was aimed at determining personal hygiene practice level and its associated factors among elementary school grade (5–8) students in Fiche town, Oromia, Ethiopia, in 2022.

A cross-sectional study design was conducted from April 29 to May 29, 2022, in Fiche town, Oromia regional state, among 534 elementary school students. A multi-stage probability sampling technique was used to select the individual students. A structured questionnaire was used to collect the data. The data was entered into epi-data version 4.6 and analyzed by SPSS version 26.0. Variables that scored a p-value less than 0.2 during bivariate analysis were included in multilevel logistic regression models to determine factors associated with personal hygiene practice. The odds ratio with a 95% confidence interval was estimated, and the level of significance was set at \(\:\le\:\) 0.05.

The magnitude of good personal hygiene (scored above the mean) was 59.2% (95% confidence interval (CI)) (55.1–63.0). A considerable proportion of students scored more than 50% in latrine use (62.5%), regular hand-washing (55.4%), and oral hygiene (55.20%) practices. Being female, having good personal hygiene knowledge, doing hygiene inspections at school, and having latrine accessibility was significantly associated with good personal hygiene among elementary school students.

Considerable proportion of elementary school students in Fiche town have score poor personal hygiene practice. Interventions aimed that target improving knowledge of personal hygiene and hygiene inspection at school are crucial to enhance the personal hygiene among elementary school students.

Peer Review reports

Introduction

The term “hygiene” refers to the practice of keeping oneself and one’s surroundings clean, mainly in order to avoid illness or disease spread [ 1 , 2 , 3 ]. Hygiene is the process of cleansing an environment of any pathogens that could cause illness [ 4 ]. The majority of health problems affecting school students can be prevented by encouraging personal hygiene (PH) practices among schoolchildren and family members. Poor school sanitation and personal hygiene are the main problems with school setup, and it is still a high-risky habit among elementary school students [ 2 , 4 ]. The majority of diarrheal disease-related illnesses could be avoided if schools had a reliable, safe water supply and good sanitation practices [ 2 , 4 ].

Globally, there are 2.4 billion people who live without adequate sanitation; 758 million do not have access to improved water sources; and 673 million still defecate in the open field [ 5 ]. Beyond the immediate implications for the child’s health, poor HP in children can have major economic and social effects, including significant school absences; the spread of infectious agents to others; and lost workdays for parents and guardians. Around 1.9 billion educational days are lost due to sickness each year globally on average due to sickness that could be prevented [ 2 , 4 ].Water-related illnesses account for approximately 443 million school days missed each year in the developing world, making them a major cause of school absences [ 6 ].

Over two million people die each year from diarrheal illnesses, with children being more at risk of dying from these infections [ 7 ]. Over 80% of diseases are linked to poor hygiene in underdeveloped countries [ 7 ]. Poor water, sanitation, hygiene (WASH) accounts for 60% of the burden of communicable diseases (CD) in Ethiopia, and over 250,000 children die yearly [ 6 ]. As a result, CDs are considered the major causes of illness, death, and disability in Ethiopia. Schools with poor hygiene and intense person-to-person contact are highly risky environment for children [ 6 ]. However, few schools in Ethiopia have a water supply and toilet facilities for sanitation and hygiene purposes [ 8 ].

Despite considerable evidence on PH problems among general population in Ethiopia, there is an evidence gap on PH among elementary school students. Moreover, there are limited evidence regarding personal hygiene practices among elementary school students the study area. In addition, students are at greater risk of acquiring diarrheal diseases, acute respiratory infections, and other personal hygiene-related diseases in schools. However, there is limited information on the factors affecting personal hygiene in elementary schools. Therefore, this study was aimed to determine the magnitude of personal hygiene and associated factors among elementary school students in Fiche town.

Methods and material

Study design and setting.

An institution-based cross-sectional study design was used to determine personal hygiene practice and its associated factors among elementary school students in Fiche Town, Oromia region, Ethiopia. There were 13 primary schools in the town. Of these, eight were grade 5–8 schools, while five were grade 1–4 schools. Based on the data obtained from the education bureau, of the 9292 primary school students, 4818 were in grades 5–8 and enrolled in school for 2021/22 academic years. This study was conducted in elementary schools in Fiche town from April 29 to May 29, 2022, among all students who were in the secondary cycle (grades 5–8).

Inclusion and exclusion criteria

All grade 5–8 students who admitted for 2021/22 academic year were included in the study. However, mentally and physically incapable students were excluded from the study.

Sample size determination

The sample size was calculated using a single population proportion formula by assuming 30% true population prevalence of good personal hygiene practice among the students [ 6 ], 5% margin of error, 95% confidence interval, and 1.5 design effect. Accordingly, the determined sample size was 323 students. By accounting for the design effect within the clusters (schools and grade) the sample size was increased by 1.5 design effect and the total sample size became 485 students. The sample size further increased by 10% for non-response rate and the total sample size of this study was 534 secondary cycle students.

Sampling procedure

A multi-stage probability sampling method with three stages was used. The first stage was schooled; the second classes; and the third individual students. There were 13 elementary schools in Fiche town; of these, eight schools had a full cycle from grade 1–8. Five schools were selected from the total 13 schools by a simple random sampling method. Of the total 3769 students who were enrolled in grades 5–8 in the 2021/22 academic year, 534 students were selected by proportion of the total number of students in school, and each student was selected by a simple random sampling method using a list of students’ names in each section as a sample frame [Fig. 1 ].

Schematic representation of the sampling procedure of students Fiche town, Oromia, Ethiopia, 2022

Data collections tools and methods

A structured questionnaire was prepared based on a literature review [ 1 , 6 , 9 , 10 , 11 ]. It was prepared in English and translated into the local languages (Afan-Oromo and Amharic). The two-day training was provided for five data collectors and supervisors on the study objective, procedure, research ethics, and data collection tools. The students were selected by five teachers, who were school supervisors. After individual students were selected, study objectives and procedures were thoroughly explained for each selected student. Assent was obtained from each family of the student (by sending consent forms to their family) for those younger than 18 years, and written informed consent from students who were older than 18 years. Finally, the structured questions were administered by trained data collectors. The data collection process was supervised by the principal investigator and supervisors.

Data analysis

The data was entered into Epi-Data, cleaned, and recoded. Data was exported to SPSS (Statistical Package for the Social Sciences) version 26 for analysis. Descriptive statistics such as frequency and percentage for categorical variables and mean with standard deviation for continuous variables were conducted. Data are presented in text, tables, and graphs. Multilevel logistic regression models were used to assess the factors associated with poor personal hygiene practices. A multilevel logistic regression analysis was applied to account for the corrections at the school, class, and individual levels. It also enables the partitioning of the total variation in the outcome within groups and between school, class, and individual variances by modelling cross-level interaction [ 12 ]. The first level was a school; the second level was classes; and the third level was individual student behaviour. Variables with a p-value ≤ 0.2 during bi-variable analysis were included in the multivariable model by the stepwise model-building method. Multi-collinearity between independent variables was checked by a variance inflation factor (VIF). Model fitness was checked by the Hosmer and Lemeshow goodness-of-fit tests. Adjusted odds ratios with 95% confidence intervals were estimated to show the strength and significance of the association between each independent and dependent variable. P \(\:\le\:\) 0.05 was used as a significant association.

Socio-demographic characteristics of participants

From five elementary schools, 534 students were participated in this study with a response rate of 100%. Of 534 participates, 227 (42.5%) were male. The mean age ± standard deviation of the participants was 14.3 \(\:\pm\:\) 1.7 years with the age range of 9 to 22 years. From the total of 534 students, grade five 91(17%), six 159 (29.8%), seven 139 (26%) and eight145 (27.2%) [Table 1 ].

Knowledge of personal hygiene

The majority of the students got personal hygiene information from their families 332 (65.4%). Nearly half (52.2%) of the students had good knowledge of personal hygiene, while 365 (68.5%) had good hand washing, and 449 (84.1%) had good oral hygiene. The majority of the students (84.1%) knew that hand washing is necessary before eating food, and 352 (65.9%) after defecation and 322 (60.4%) after eating food. The majority (90.1%) of elementary students understood cleaning teeth with a chewing stick/toothpaste and brush to prevent tooth decay and the unpleasant odor of breathing [Table 2 ].

Magnitude of personal hygiene practice

More than half of the students had good hygiene practices, while 318 (59.60%) had good hand washing practice [Fig. 2 ]. Almost all (98.7%) elementary school students were practicing regular bathing. Of the students who took a bath, the majority (76.1%) took it once a week. Most (83.1%) of the students have experience of hand washing with soap or ash. The majority of the students (88.4%) brushed their teeth; of those who brushed their teeth with a brush and soap, 331 (62.0%) and only 147 (27.5%) brushed twice per day (morning and night). Almost all (97.6%) students washed their faces. Among those who washed their faces, 247 (46.3%) washed with soap twice a day, and 520 (97.4%) trimmed their nails regularly [Table 3 ].

Magnitude of hygiene practice of elementary school students in Fiche town, Oromia, Ethiopia, 2022

About two thirds (65.5%) of the students stated that there was a weekly personal hygiene inspection in school. All elementary schools had latrine facilities in their compound, but the available latrines were not adequate for the number of students (i.e., the toilet to setting pit ratio was 0.009 for females and 0.008 for male students). One-fourth of the students practiced open field defecation.

The majority (87.1%) of students have received health education on personal hygiene which given by teachers (81.7%), health professionals (32.3%), non-governmental organizations (6.9%), school clubs (23.4%), and media (23.9%). Most (70%) of the students participated in hygiene-related clubs such as sanitation and hygiene (40.4%) and menstrual hygiene clubs (40.8%) [Table 4 ]. About two third (65.5%) of the students were stated as they had weekly personal hygiene inspection. Among the 401 students, 394 (73.8%) washed their hands after eating and 365 (68.4%) washed their hands after using the toilet. Nearly half of the students had hand washing practice after critical time [Fig. 3 ].

Shows the percentage distribution of (Use soap/ash during hand washing before eating ( A ), Always wash hands with soap/ash after eating ( B ), Always wash hand with soap/ash after visiting toilet ( C ) and hand washing after critical time ( D ) in Fiche town, Oromia, Ethiopia, 2022

The children in this study area had diarrhea the last two weeks before data collection 43(8.1%) and headaches 86(16.1%) (Fig. 4 ).

Shows that students having illness before the last two weeks of data collection among elementary school students in Fiche town, Oromia, Ethiopia, 2022

Factors associated with personal hygiene practice

Being female students (COR = 1.9, 95% CI (1.3– 2.7); p < 0.001), having mother who attended primary and secondary school (COR = 2.1, 95% CI (1.4 − 3.1); p = 0.001) and Diploma or above (COR = 1.9, 95%CI (1.1–3.2), p = 0.013) were significantly associated with personal hygiene practice Family size less than or equal to five (COR = 1.8, 95% CI (1.3–2.6), p = 0.001), Being received health education on personal hygiene (COR = 3.2, 95% CI: 1.9–5.4; p < 0.001), being participated in health-related clubs (COR = 2.1, 95% CI (1.4–3.0); p < 0.001); and being trained in personal hygiene (COR = 1.5, 95% CI(1.1 − 2.2); p = 0.017) were significantly associated with personal hygiene practice in unadjusted analysis. Moreover, availability of school personal hygiene inspection (COR = 2.1, 95% CI (1.5–3.0, p < 0.001), having good knowledge on oral hygiene, (COR = 2.0, 95% CI (1.3 − 3.2); p < 0.000), hand washing (COR = 2.2, 95% CI (1.5 − 3.1); p < 0.001), and personal hygiene (COR = 2.4, 95% CI (1.7 − 3.4); p < 0.001) were significantly associated with personal hygiene [Table 5 ].

In multivariate multilevel logistic regression model, being female student (AOR = 1.8, 95% CI (1.1 − 2.8); p = 0.013), availability of school personal hygiene inspection (AOR = 1.9, 95% CI (1.1 − 3.2); p = 0.015), and good knowledge towards overall personal hygiene (AOR = 2.3, 95% CI (1.3 − 4.1); p = 0.005) were significantly associated with good personal hygiene practice [Table 5 ].

This study was conducted to determine personal hygiene practices and their associated factors among elementary school (grades 5–8) students. It revealed that, more than half of the students had a good overall personal hygiene (PH), hand washing (HW), latrine use (LU), and oral hygiene (OH) practices. Personal hygiene knowledge, hygiene inspection in school, and being a female student were significantly associated with personal hygiene practice.

The magnitude of overall good PH was 59.2%, which was higher than the findings of a similar study reported from Mareko District [ 6 ]. This discrepancy could be due to the level of knowledge of children about personal hygiene and the fact that the residence of the previous study was only in town. However, in the current study, the students resided in both urban, semi-urban, and rural areas, which could have an effect on personal hygiene practices. In contrast, the results of the current study are similar to those of the previously reported studies [ 13 ]. In the present study, the overall personal hygiene knowledge of students was half, which was higher than the survey study reported by rural students from China [ 14 ]. This difference may be due to the setting of the study. In the current study, the students were residents of mixed setups, while the participants in the study reported from China were purely rural residents [ 14 ].

In the current study area, all elementary schools had toilets, compared with the national minister of education’s report (2017) that 76% of schools in Ethiopia have latrines [ 15 ]. In the current study area, all elementary schools had toilets, compared with the national minister of education’s report (2017) that 76% of schools in Ethiopia have latrines [ 15 ]. In the present study, good LU practice was found to be 62.5%. This finding was higher than the findings of a previous study reported from Mareko District, in which 46% of students practice LU [ 6 ]. Moreover, the present study result on latrine use practice was higher than the previous study reported from Chencha District (33.3%) [ 16 ] and Sigmo (39%) [ 17 ]. The availability of separate toilets by sex (48.0%) and toilet privacy (30.8%) were the main motivators that encouraged students to use the toilet in the present study. This result is in agreement with to the study reported by Mareko 50% [ 6 ]. The result shows that the students stated that 33.1% of the school latrines were inaccessible to students irrespective of their physical disabilities, and 66.9% of the school children stated latrines were not accessible to younger students. This could be due to the design problem (21.8%), the distance from the rooms (12.6%), or the fact that 222 (62.2%) had no reason.

In the current study, hand-washing facilities near the toilet were 38.4% higher compared to the national minister of education’s report of 4.4%. This might be due to the fact that the study area is smaller than the national survey. Good hand washing practice among elementary school children in Fiche town was found to be 59.6%. This is very high compared with a study in Mareko (23%) [ 6 ], Yirgalem Town (39.1%) [ 7 ], Debark Town (52.2%) [ 18 ], Arba Minch Town (22.3%) [ 19 ], and Sebeta Town (32%) [ 20 ]. This could be due to the availability of sanitation facilities in the study areas. However, the present study result is similar to a study reported from India (60%) [ 21 ]. More than half (59.7%) of the students were always washing their hands with soap or ash at critical times. This result was lower than the results reported in studies conducted in Yirgalem town (88.2%) [ 7 ], Bangladesh (71.6%) [ 22 ], and the United Arab Emirate (71%) [ 23 ]. However, the present study result is higher than the studies reported from Mareko (26.8%) [ 6 ] and India (29.1%) [ 24 ]. This difference is most probably due to the difference in the knowledge level of the students about hand washing.

Two-thirds of the students had good knowledge of handwashing practices. This was similar to the study reported from Hosanna town (66.1%) [ 25 ]. However, the result of the current study on knowledge of washing hands with soap is much lower than study reported from Yirgalem (89%) [ 8 ], Bangladesh (89%) [ 22 ] and Saudi Arabia (90%) [ 3 ]. This difference most probably due to the high sample size used in the current study and the educational status of the family.

The proportion of oral hygiene knowledge among the students was 84.1%. However, among elementary school students in Fiche town, good oral hygiene practice was 55.2%. This result was higher than the previous studies reported from different settings. For instance, the studies reported from Ghana (79.9%) [ 13 ] and India (70.4%) [ 26 ], in Southeast Serbia (54.5%) [ 27 ] reported a lower proportion of oral hygiene knowledge. This difference might be due to sample size and oral hygiene-related culture in different study areas.

Almost half (53.2%) of the students were brushing their teeth once a day. The students who brushed their teeth for less than 60 s were 47.9%, which is Debre Tabor [ 28 ]. At Fiche Town Elementary School, 27.5% of students brush their teeth twice a day. This result was much smaller than a study conducted in Saudi Arabia in which 71.7% of elementary school students brushed their teeth [ 3 ]. This difference could be due to differences in study area culture, economic status, and sample size.

Female students were 1.8 times more likely to have good hygiene practices compared with male students. This result was supported by the fact that male students are 0.42 less likely to have good personal hygiene practices in Côte d’Ivoire [ 29 ] and in Bangladesh [ 30 ]. The majority (98%) of men and women agree that washing hands after toileting is important [ 31 ]. Moreover, 91% of women and 84% of men are more likely to report the importance of handwashing after toilet use [ 31 ].

The students who had good knowledge of personal hygiene were 2.3 times more likely to have good personal hygiene practice compared with those who had poor knowledge, and knowledge significantly determined personal hygiene practice. The present study result is supported by a study reported by Mareko [ 32 ] in which personal hygiene practice is 5.1 times higher among those with high knowledge. Moreover, the current study findings are similar to those reported in Debark Town [ 18 ].

Diarrheal diseases alone were responsible for 43 (8.1%) of the school absences in the present study. The current study result is smaller (28.8%) than the results of the study reported by Mareko [ 6 ]. This is most probably due to the water treatment with chlorine 381 (71.9%) and the study area and time. In this study, almost one-third of the elementary school students were suffering from one or more morbidities related to poor personal hygiene practices in the past two weeks.

The nature of the study design and the self-reported data collection tools recall bias (remember the last two weeks of illness and the last dental follow-up). The cross-sectional study design means that because exposure and outcome are simultaneously measured, there is generally no evidence of a temporal relationship between exposure and outcome, which could not enable us to investigate the cause-and-effect relationship.

The overall personal hygiene practice among elementary school children in the study area was minimal. Innervations that would be implemented by schools, teachers, health extension workers, and WASH project officers are required to raise knowledge on personal hygiene practice among elementary students and increase the availability of regular personal hygiene inspections. The availability of personal hygiene facilities at home and in school is crucial to promoting personal hygiene practice. Further research that triangulates quantitative and qualitative data is recommended for a holistic understanding of the problem.

Data availability

All munscript data was there with authors (collected data SPSS result and full research data).

Abbreviations

Adjusted Odd Ratio

Communicable Disease

Confidence Interval

Crude Odd Ratio

Demographic Health Survey

Hand washing practice

Latrine utilization practice

Oral hygiene Practice

Personal Hygiene

Statistical package for Social Science

Water and Sanitation Hygiene

World Health Organization

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Acknowledgements

The authors would like to acknowledge Salale University for funding this study. We would also like to acknowledge the contribution of the Fiche town education office and all selected school administrations for their cooperation and support during data collection. We also appreciate the toleration and cooperation of all data collectors and participants.

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Getaneh Haile Minda, Habiteyes Hailu Tola, Asefa Kebie & Tewodros Endale

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GHM- Conceptualization, data curation, formal analysis, investigation, funding acquisition, methodology; AFA, AK, TE- data curation, writing a review and editing the manuscript; HHT- Conceptualization, formal analysis, investigation, funding acquisition, methodology, project administration, resources, software, supervision, validation, visualization, writing a review and editing the manuscript.

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This study was ethically approved by the Institutional Review Committee (IRC) of Salale University on March 20, 2022 (Ref. No. 878/2022). Written informed consent was obtained from each student older than 18 years, and assent was obtained from families of students younger than 18 years. All information collected was recorded anonymously and confidentially.

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Minda, G.H., Tola, H.H., Amhare, A.F. et al. Personal hygiene practice and associated factors among elementary school students in Fiche Town, Oromia, Ethiopia. BMC Infect Dis 24 , 781 (2024). https://doi.org/10.1186/s12879-024-09665-7

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The hygiene hypothesis is a "dangerous misnomer which is misleading people away from finding the true causes of these rises in allergic disease," says Sally Bloomfield, chair of the International Scientific Forum on Home Hygiene and an honorary professor at the London School of Hygiene and Tropical Medicine. "I've even seen things in ...
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The Hygiene Hypothesis. The "Hygiene Hypothesis" is a theory that suggests a young child's environment can be "too clean" to effectively stimulate or challenge the child's immune system to respond to various threats during the time a child's immune system is maturing. As a fetus, the immune system is thought to be repressed to avoid rejecting ...
The hygiene theory: fact or fiction?
The hygiene hypothesis remains a credible but nonspecific explanation for observed variations over time, place and persons at risk for developing atopic allergic disorders. More prospective studies are needed to unravel which infectious agents exert a protective effect and the time period of importa …
The 'hygiene hypothesis' for autoimmune and allergic diseases: an
The hygiene hypothesis is based upon epidemiological data, particularly migration studies, showing that subjects migrating from a low-incidence to a high-incidence country acquire the immune disorders with a high incidence at the first generation. However, these data and others showing a correlation between high disease incidence and high socio ...
What is the hygiene hypothesis?
What is the hygiene hypothesis? by Bianca Nogrady. The idea that we need to be exposed to germs and bacteria in early childhood is the subject of much debate, but what is the hygiene hypothesis?
What is the Hygiene Hypothesis?
The hygiene hypothesis is a proposed explanation for why allergies and asthma are now epidemic, especially in developed countries where most kids live in relatively sanitized environments. Recent research from the U.K.'s University of Cambridge suggests that the hygiene hypothesis may also account for higher rates of Alzheimer's disease in ...
The Hygiene Hypothesis and Autoimmune Disorders
The hygiene hypothesis is a hypothesis that suggests that the increased incidence of allergic and autoimmune disorders are linked to the tremendous changes in sanitation standards and practices ...
What exactly is sleep hygiene
Sleep hygiene, much like regular hygiene, isn't a one and done kind of activity. Consistency is key. Just like you should brush your teeth every morning, you should commit to sleep hygiene every ...
Personal hygiene practice and associated factors among elementary
The term "hygiene" refers to the practice of keeping oneself and one's surroundings clean, mainly in order to avoid illness or disease spread [1,2,3].Hygiene is the process of cleansing an environment of any pathogens that could cause illness [].The majority of health problems affecting school students can be prevented by encouraging personal hygiene (PH) practices among schoolchildren ...

Is the Hygiene Hypothesis True?

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What Is the Hygiene Hypothesis?

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Can It Be Bad to Be Too Clean?: The Hygiene Hypothesis

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The hygiene hypothesis: How being too clean might be making us sick

How doctors got the idea that dirt could make us healthy

The evidence for the hygiene hypothesis

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Is Being Too Clean Bad for Your Health?

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Research Materials

The ‘hygiene hypothesis’ for autoimmune and allergic diseases: an update

Introduction

Evolving epidemiology of allergic and autoimmune diseases

The decreasing incidence of infectious diseases

Uneven distribution

Search for risk factors at the origin of the increase of immunological disorders

Epidemiological data indicating a direct link between the decreasing level of infectious burden and the rising incidence of immunological disorders

Proof of principle of the causal relationship between decline of infectious diseases and increase of immunological disorders

Animal models

Increased atopy after anti-parasitic treatments

Prevention of allergic and autoimmune diseases by infections

Is there a role for microbiota changes in the hygiene hypothesis?

Mechanisms of the hygiene hypothesis

T helper type 1 (Th1)–Th2 deviation

Antigenic competition /homeostasis

Immunoregulation

Non-antigenic ligands

Gene–environment interactions

Therapeutic strategies

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