Review of Hygiene Hypothesis for Allergies

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Table of Contents

Introduction
Brief History of Hygiene hypothesis
Mechanisms of action
Hygiene hypothesis and the specific nature of the immune system
Conclusion
References

Introduction

Unlike in the past, people are now increasingly becoming aware about ways that they could use to keep the disease-causing germs at bay. Airtight doors and windows, anti-bacterial soaps, strong antibiotics, and vaccinations have been developed to keep these germs at bay. Majority of the people, especially in developed countries are aiming at cleanlier lifestyles. But according to Bloomfield et al. (2006), while living a germ and dirt-free life can thwart some of the life-threatening infections and diseases, leading cleanlier way of life can be related to an observed increase in allergies among the little children. In a layman’s language, this is what is referred to as the hygiene hypotheses. Before we developed all these instruments of fighting germs and dirt, our bodies had a natural mechanism of fighting the germs. This was in the name of a strong immune system. This is no longer the case. Due to the tendency to live cleanlier lifestyles, our immune systems tend to develop more allergic tendencies rather that fight infections (Liu & Murphy, 2003).

According to Norton (2008) and Singer (2008), hygiene hypothesis comes about when non-exposure to allergens, germs, and parasites weakens the human immune system and increases individuals’ vulnerability to allergic infections. According to Gibbs et al (2004), the concept that non-exposure to infections in early life leads to the development of Atopic disease has come to be referred to as hygiene hypothesis. Braun-Fahrlander (2002) has attempted to relate the lower prevalence rates of childhood asthma in Bangladesh, in relation to developed countries, to the hypothesis. According to hygiene hypothesis, western lifestyles, characterized by lower rates of infections, higher level of hygiene, and smaller family size have contributed to the high prevalence of asthma in Western countries.

Brief History of Hygiene hypothesis

According to Bloomfield et al. (2006), an article published in the British Medical Journal in 1989 by David P. Strachan first proposed the concept of hygiene hypothesis. An observation was made that some allergic infections such as eczema and hay fever were less frequent in children from big families. During this time, it was presumed that children from larger families were more exposed to infectious agents due to the size of the family, than in children from smaller families. This line of thinking brought about the hygiene hypothesis (Carpenter, 1999).

From that time onwards, hygiene hypothesis has become a vital theoretical framework in the analysis of allergic disorders as it continues to be widely investigated by epidemiologists and immunologists. This concept has time and again been used by scientists to offer explanations about the high prevalence of allergic infections especially in developed countries since the industrialization era. According to Bloomfield et al. (2006), the concept has now been enlarged to include exposure to parasites and symbiotic bacteria as “crucial modulators of immune system development, along with infectious agents.”

Mechanisms of action

To better understand the concept of hygiene hypothesis, it is only imperative to understand how it works. A TH2 mediated immune response, often brought about by inappropriate immunological responses brings about allergic reactions and infections. According to Carpenter Hypothesis (1999) and Schena (2007), a TH1 mediated immune response is often elicited by many viruses and bacteria, thus down-regulating TH2 responses. Accordingly, the first proposed mechanism of action to hygiene hypothesis stated that overactive TH2 arm, which led to allergic infections, was brought about by inadequate stimulation of the TH1 function of the immune system. But this mechanistic explanation failed to explain the rise in occurrence of several TH1 mediated autoimmune infections namely, multiple sclerosis (MS), Inflammatory Bowel Disease (IBD), and type 1 diabetes.

According to Singer (2008), alternative mechanistic explanation argues that “the developing immune system must receive stimulus from parasites, symbiotic bacteria, or infectious agents to adequately develop regulatory T cells, or otherwise become more susceptible to autoimmune diseases and allergic infections because of the insufficiently repressed TH1 and TH2 responses.”

Hygiene hypothesis and the specific nature of the immune system

As discussed above, immunological research at the time hygiene hypothesis was first proposed supported the idea that a naïve immune system was more likely to overreact to more benevolent objects found in the environment. A naïve immune system is one that has not been adequately challenged by parasitic or infectious organisms (Gelfand, 2003,). This explains the belief held during that time that people who aimed at living cleanlier lifestyles were more likely to develop allergic diseases. But subsequent researches have shown that this could be further from the truth. It is now official that parasites and bugs are not necessarily the causative agents of allergic infections. Allergic infections occur due to “lack of certain organisms that have, over the course of evolution, trained our immune system to be more tolerant” (Gelfand, 2003). This therefore shows that hygiene hypothesis must be rethought.

In trying to understand the link between allergic and infectious diseases, researchers put their focus on only one component of the immune system, namely the T-helper (TH) cells. Apart from having a role in autoimmune disease, the TH1 cells also fights viral and bacterial infections. In their roles, the TH2 cells mediate allergic reactions and deals with parasitic infections. The argument previously advanced was that decreased exposure to micro-organisms due to increased observance of hygiene failed to prime the TH1 response, therefore leading to the overcompensating of TH2 activities. This led to allergies (Gelfand, 2003).

However, a reverse hypothesis was produced by scientists working in the area of autoimmunity. In this area, diseases are often mediated by TH1 lymphocytes. Their investigations revealed that non exposure to pathogens caused inadequate TH2 activity. More TH2 activity was needed for the TH1 activity to be down-regulated. Lack of this down-regulation caused type 1 diabetes, multiple sclerosis, and Crohns disease (Gelfand, 2003; Fendt et al. 2005). This shows that hygiene hypothesis is contrary to the specific nature of the immune system basically because autoimmune diseases such as inflammatory bowel disorders and type 1 diabetes are as prevalent today as the allergic disorders such as asthma. An experiment that was carried out by Gibbs et al. (2004) found out the evidence supporting the hypothesis is inconsistent to date. In the experiment, the found out that amplified exposure to infections cannot in any way explain the reduced risk of Atopic disease.

According to Norton (2008), immunities are bestowed upon us by our mothers in the form of antibodies. These antibodies are passed through the placenta and also by breastfeeding. Depending on what we are exposed to, our immune system matures and learns how to function. The immune system fights the diseases and infections through the production of antibodies. Though the invading organisms mutate over time, exposure to them means that the immune system will produce more anti bodies. Allergic reactions come into focus when our immune system get confused and start forming antibodies against non-harmful agents by nature. To this end, the hygiene hypothesis tried to explain that allergies develop due to the immune system developing fewer antibodies due to living in a sanitized environment. According to its basic propositions, living in a serine environment may weaken the immune system, thus causing unsuitable immune reflexes exhibited in assaulting harmless substances such as pet dander, pollen, latex, and certain food proteins (Holt, 2008).

But Carpenter (1999) and Bloomfield et al (2006) uses the investigations conducted by Dr. Marc Rothenberg and associates to deny hygiene hypothesis proposition. Their experiments, conducted on mice concluded that some white blood cells named eosinophils were the likely cause of gastrointestinal inflammation and numerous food allergies. These white blood cells identify some food proteins as harmful germs in individuals suffering from food allergies. When an allergen is exposed to the intestinal lining of an allergic individual, a compound called eotaxin is discharged. This causes the white blood cells – eosinophil and other immune cells to assault them and discharge powerful proteins, thus destroying immediate tissues and causing eosinophilic irritation. This argument serves to further show that hygiene hypothesis for allergies seem contrary to the specific nature of the immune system.

To criticize the theory further, it can be argued that the popular interpretation being proposed by hygiene hypothesis, that dirt is good for us has considerably influenced the attitudes and beliefs of many people to a point of making the public lose confidence regarding home hygiene. According to Bloomfield et al. (2006), clear guidelines must provided explaining how dirt is different from germs. This will go a long way in protecting people from contracting other dangerous diseases on the premise of strengthening their immune systems.

Hygiene hypothesis seem to address the specific nature of the immune system in as far as the above is concerned. It tries to compare the rise of allergic infections, more so, in the developed world with the change in lifestyles. We no longer expose ourselves to the germs that make our immune system to function better. To this extent, our immune systems react to foreign substances it deems harmful, therefore causing allergies. Such foreign substances include dust and dust mites, pollen, mold, insect stings, animal dander, and certain types of foods. But in as far as the hygiene hypothesis may try to address the specific nature of immune system; it fails to give a definitive evidence for the reasons behind the sudden increase in some specific forms of allergic reactions such as food allergies, according to Groce (2007) and Yano et al. (2005). The main premise of hygiene hypothesis is that our immune system’s opportunity to develop standard immune responses have been severely curtailed by the decreased exposure to germs and other infection-causing organisms as a direct result of modern western lifestyles. But this proposition fails to address the fact that the immune systems of people in the third world, where people are continuously exposed to disease-causing germs seems as susceptible to allergic infections as those of people from the developed countries. To this extent, the hygiene hypothesis is contrary to the specific nature of the immune system.

According to Groce (2007), the extent to which can address the specific nature of the immune system still remains a matter of debate. The presence or absence of certain types of helpful bacteria that usually resides in the small intestines forms one of the differences in areas affected by the hygiene hypothesis. The effects of early exposure to certain infectious infections as well as exposure to parasites also bring varying trends on how hygiene hypothesis affects various individuals. According to Braun-Fahrlander (2002), though hygiene hypothesis may in part explain to explain the lower prevalence of asthma in Bangladesh compared to western countries, it fails to address why asthma prevalence in Bangladesh is still substantial enough to constitute an important health concern. Disparities in allergic infections between individuals with varying lifestyles and who resides in different parts of the world continues to exist, therefore meaning that hygiene hypothesis alone cannot be enough to explain the occurrence of allergic infections. Other factors must come into play.

Umetsu (2004) reporting in Nature Medicine said that the evidence for hygiene hypothesis remains too sparse and circumstantial for majority of the scientists to be convinced. But scientists have been working on the “assertions” that when the immune systems lacks the know-how and practice to fight viruses and bacteria, infections can occur. However, no substantial evidence has been constructed, at least according to Umetsu. This therefore proves our thesis that the hygiene hypothesis for allergies seems contrary to the specific nature of the immune system.

Conclusion

According to Carpenter (1999), “the radical notion that infrequent exposure to infectious agents contributes to autoimmune diseases has generated far more controversy than the idea that allergies and asthma stem from such deprivation.” Infact, according to most scientists, the opposite is true. Majority hold the view that autoimmune diseases are driven more by infections. To punch holes on the hygiene hypothesis, other scientists are of the view that other environmental factors, including environmental toxins most likely prompt autoimmune reactions more than the hygiene hypothesis. Ultimately, though scientists aren’t yet ready to accept the hygiene hypothesis proposition, it may be that “allergies, asthma, and other immune disorders are the price society has to pay for escaping the appallingly virulent infectious infections that have struck down children over the centuries”, at least according to Carpenter (1999).

References

Bloomfield, S.F., Stanwell-Smith, R., Crevel, R.W.R., & Pickup, J (2006). “Too clean, or not too clean: The hygiene hypothesis and home hygiene.” Clinical and Experimental Allergy, Vol 36, no. 4, pp 402-425. Web.

Braun-Fahrlander. (2002). “Does the hygiene hypothesis provide an explanation for the relatively low prevalence of asthma in Bangladesh?” International Journal of Epidemiology, vol. 31, pp 488-489. Web.

Carpenter, S. (1999). “Modern hygiene dirty tricks: The clean life may throw off a delicate balance in the immune system.” Science news, vol. 156, no. 7. Web.

Fendt, J., Hamm, D.N., Banla, M., Schulz-Kay, H., Wolf, H., Helling-Giese, G., Heuschkel, C.,& Soboslay, P. (2005). “Chemokines in Onchocerciasis patients.” Clinical and Experimental Immunology, vol. 142, no. 2, pp 318-326. Web.

Gelfard, E.N. (2003). “The hygiene hypothesis revisited: Pros and cons.” Medscape Today. Web.

“Genes essential to the immune system that are entrusted to microbial old friend.” (2008). The Evolution and Medicine Review.

Gibbs, S., Surridge, H., Adamson, R., Cohen, B., Bentham, G., & Reading, R. (2004). “Atopic dermatitis and the hygiene hypothesis: a case control study.” International journal of epidemiology, vol. 33, no. 1, pp 199-207. Web.

Groce, V. (2007). What is Hygiene Hypothesis? Web.

Holt, B. (2008). Hygiene Hypothesis: Are we too clean? Knoll. Web.

Liu, A.H., & Murphy, J.R. (2003). “Hygiene hypothesis: Fact or fiction.” Journal of Clinical Immunology, 111(3):471-8.

Norton, A. (2008). “Are we scrubbing away our immune system and giving ourselves allergies.”

Squiddo Health and Medicine. 2008. Web.

Schena, L.B. (2007). “Getting the dirt on germs.” USC Health magazine. Web.

Singer, E. (2008). “The new hygiene hypothesis: The Microbes within us could explain raising allergy rates.” Technology Review. Web.

University of Michigan Health System. (2007). “The Hygiene hypothesis: Are Cleanlier lifestyles causing more allergies for kids?” Sciencedaily. Web.

Umetsu, D.T. (2004). “Flu strikes the hygiene hypothesis.” Nature medicine, vol. 10, pp 232-234. 2008. Web.

Yano, H., Shiiba, D., Kozai, H., & Kato, Y. (2005). “The hygiene hypothesis and exercise: Does exercises prevent allergic disorders.” Kawasaki Medical Welfare Journal, vol. 15, no. 1, pp 1-11. Web.

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