Providing a definitive answer to the question, “In what way are my allergies a result of nature or nurture?” is not currently possible. In reality, unraveling the precise role played by nature (genetics i.e. hereditary factors) or nurture (environment and other non-hereditary factors) in allergic conditions is significantly more complex and less well understood than implied by the common definition of the term ‘atopy’ i.e. a genetic predisposition to Type 1 Hypersensitivity involving IgE to environmental allergens.
The Case for Nature and Hereditary Factors in Allergies
The notion that allergies appear to run in families appears to have merit based on various studies, although our understanding is still far from complete at the present time. For example, the risk of a child developing asthma increases if one parent has the condition but significantly more so when both parents are affected (Litonjua et al. 1998). However, Burrows et al. 1995 previously noted that elevated IgE levels in asthmatic children were higher than would have been expected based purely on parental IgE levels. The study suggested such a result is compatible with “familial-aggregation hypotheses and a strong environmental influence determining which children are likely to develop asthma”.
Studies on twins – identical/monozygotic (both strands of DNA are identical) and fraternal/dizygotic (one strand of DNA is identical) – using various genetic testing and sequencing techniques provides a fascinating tool to investigate the underlying hereditary nature of allergies. In general, the occurrence of allergies amongst identical twins is significantly more so than for fraternal twins; such results strengthen the case that hereditary factors play a significant role in allergies e.g. Duffy et al. 1990, Sicherer et al. 2000.
Furthermore, research into locating the genes associated with allergies is becoming increasingly widespread. For example, the Weidinger et al. 2008 discovery of the FCER1A gene, which appears to play a significant role in allergic responses through regulating IgE production, may pave the way for new allergy drugs. Renkonen et al. 2010 suggested 39 genes related to acute allergic diseases, whereas Madore and Laprise 2010 collated various allergic diseases, prevalence and number of associated genes in a simple table form. It should be noted though, that explaining and predicting genetic susceptibility to allergic diseases using genes (and variations in them) is still in its infancy. Moreover, a number of genes originally considered not linked with allergies have subsequently been associated with them e.g. asthma and ADAM 33 (chromosome 20) Mahesh 2013.
The Case for Nurture and Non-Hereditary Factors in Allergies
Although the case for hereditary factors playing a significant role in allergies grows daily, the worldwide increase in the prevalence of various allergies and allergic asthma suggests other factors are involved in this complex condition. Considered a rare disease at the start of the 20th century, the apparent upward trend in allergies is clearly a cause for concern on both a suffering and financial level; particularly so in Western industrialized regions, which on a worldwide scale appear to be most affected. For example, Arbes et al. 2005 noted that over 50% of the US population now exhibit a positive allergy skin test, whilst the EAACI 2012 cite that 300+ million people in Europe will be affected by allergic diseases during the next decade (over 40% of the population). Anandan et al. 2009 review of numerous worldwide asthma studies found that despite isolated reports of a decline, “asthma prevalence is continuing to increase or remaining stable”, whereas Warm et al. 2013 observed a significant increase in the prevalence of “allergic sensitization to major airborne allergens as well as multi-sensitization” in relation to two population-based studies 15 years apart.
Various reasons have been suggested to account for this rise and even if some turn out to have merit, it would appear that they form but a small piece of a multifaceted puzzle. Examples cited include the overuse of antibiotics and antibacterial sprays, less babies being breast fed, changing food production methods, the use of certain pesticides and insecticides, excessive cleanliness as well as reduced levels of certain gut parasites e.g. Carvalho et al. 2006 (hygiene hypothesis), poor diet including an increased consumption of high inflammatory ingredients, sedentary lifestyles, increased stress levels and environmental pollutants such as car fumes.
Therefore, although heritable aspects appear to play a notable role in allergies (Lichtenstein and Svartengren 1997 suggested a figure of between 33-76%) and genetic factors (hereditary and associated issues of age, gender and race) may indicate the likelihood of one experiencing an allergy, variability e.g. in symptoms, can also be attributed to environmental (20-30% Gärtner 1990) and other non-hereditary factors (70 -80%). Pollution is an example of an environmental factor whereas other factors are behavioral or refer to childhood exposure to allergens, medication or infections etc.
Nature, Nurture and Allergies – A Complex Condition
Thus, atopy represents the tendency for allergy development but not allergy itself. When an individual is sensitized to an allergen, the term allergy refers to the development of symptoms through allergen contact. Even if an individual has a predisposition to become allergic through having inherited genetic traits, it does not mean they will definitely develop an allergy or that they will have the same symptoms as their parents. Numerous factors appear to come into play, such as:
- The genes or variability in genes they have acquired.
- The exposure profile to susceptible allergens e.g. age when exposed, exposure level and duration etc.
- Aggravating factors such as other irritants/allergens (e.g. pollutants, car fumes or tobacco smoke) or allergies (concurrent allergies).
Therefore, allergies and variability in their characteristics and symptoms appear to result from a highly complex and dynamic interplay between genes, environment and a variety of other factors. Interestingly, although research has linked hereditary influence with impacting specific allergies, results from Bønnelykke et al. 2013 study “confirms the theory that we primarily inherit the tendency to become allergic to one particular substance and not a specific allergy in itself.”
Research – Piecing the Jigsaw Together
Studies aimed at unraveling the role that nature or nurture play in determining allergies has increased significantly in recent years. Moreover, research delving into the genetic background of allergies is set to increase exponentially in the years ahead. This is in part due to advancements in technologies that enable genetic information to be processed on a scale previously impossible, coupled with a deeper understanding of the human genome. Also, a significant incentive to fund research comes from the potentially huge financial rewards reaped from developing better allergy treatments and possible cures.
Although funding and research into this aspect of allergies has been more extensive regarding humans than dogs, numerous canine studies have, are and will be taking place e.g. Merryman-Simpson et al. 2008, Plager et al. 2012, Spitzauer et al. 2013. Although genetic differences exist between dogs and humans, as close evolutionary relations with similar immune systems and underlying allergy mechanisms, conclusions derived from human studies may be applicable in some degree to allergies in dogs and vice versa. As pointed out on the Dog Genome Project, understanding the genome of the domesticated dog provides a “powerful new tool for understanding the human genome”.
However, as is the case when investigating any complex condition, the findings from allergy studies may not always appear congruent. For example, research has shown that children who have asthmatic bronchitis and grow up with pets such as dogs and cats are more prone to being allergic to these pets as adults. Conversely, Wegienka et al. 2011 noted that being exposed to pets in the first year of life was critical regarding gaining allergy protection later in life. Other studies have suggested continued exposure at an older age can also result in individuals becoming less sensitive.
The scientific process of trying to ‘discover the truth’ of complex conditions such as allergies will typically be non-linear and involve many a cul-de-sac along the way. The process will involve duplicating experiments in order to see whether the results stay consistent, adapting/refining follow-up experiments and developing new technologies. Peer review to assess the quality of the research undertaken will be based on best practice involving appraisal from other experts in the field, impartiality, checks ensuring validity of procedures and accuracy, and possible revisions. Moreover, differing opinions spawn new ways of thinking about the issues at hand and lead to novel studies that in turn can produce important breakthroughs. Therefore, although significant progress has been made in recent years concerning understanding the role played by genetics in allergic conditions, as was pointed out at the start of this article, answering the question “Do Allergies Result From Nature or Nurture?” or more accurately, “What is the precise role played by nature and nurture in allergies?” definitively, is still not possible.
Recent Related Studies
Examples of some recent allergy studies relevant to the ‘nature vs. nurture’ debate include:
STUDY | NATURE (Hereditary) | NURTURE (Non-hereditary) |
Koplin et al. 2012 study of environmental and demographic risk factors for egg allergies in infants concluded:
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Arshad et al. 2012 suggested the risk of childhood allergies are parent gender related i.e. boys have an increased risk of allergies if fathers (paternal) have the condition and the same for girls/mothers (maternal). The implications of this study could affect the way physicians consider childhood allergy diagnosis, prediction, prevention and treatment. | ✓ | |
Koplin et al. 2013 study finding evidence for the protective nature of Vitamin D for food allergy in infants. Insufficient Vitamin D can occur from a lack of sunlight or dietary deficiency. | ✓ | |
Warm et al. 2013 identified risk factors for allergic sensitization as being “young age, a family history of allergy and urban living”. | ✓ | ✓ |
Frischmeyer-Guerrerio et al. 2013 showed that protein signalling of Transforming growth factor–β (TGFβ) may be a contributor to allergic disorders. This opens the way for treating allergies using drugs that inhibit TGFβ signaling e.g. hypertensive drug Losartan. | ✓ | |
Bønnelykke et al. 2013 indicated 10 genes closely linked to allergy development and suggested hereditary impacts being allergic to a specific substance and not a specific allergy. | ✓ | |
Azad et al. 2013 supports the view that environmental exposure may be responsible for rise in allergic diseases through impacting gut microbiota. | ✓ | |
Bønnelykke et al. 2013 identified 5 asthma susceptibility genes including the newly discovered CDHR3 gene. | ✓ | |
Fall et al. 2015 supports the notion that exposure to dogs and farm animals during the first year of life reduces the risk of childhood asthma. | ✓ |