For decades, experts have known that asthma runs in families. In a recent study published in Clinical & Experimental Allergy, Randi J. Bertelsen, PhD, Department of Clinical Science, University of Bergen, Norway, and coauthors found an association between asthma and hayfever in offspring and parental bronchial hyper-responsiveness (BHR) and specific IgEs.
“Epigenetic mechanisms appear to be involved in transmission of immunological profiles from parents to offspring,” the authors wrote, “and immunological activity may modify epigenetic characteristics, as has been reported for airway inflammation in animal models.”
In this cohort study, researchers analyzed data from 4,293 adults (47% men); average age was 34 years. They also analyzed data from 9,100 of their offspring born between 1972 and 2012.
Participants in this study were part of the European Community Respiratory Health Survey (ECRHS), a random, population-based, multicenter, cohort study. Participants were recruited between 1991 and 1993, and were given an initial screening questionnaire.
A random subsample of participants in ECRHS received more extensive oral questionnaires, and clinical examinations, including the following:
- Methacholine challenge test
- Blood sampling for total and specific IgE toward common inhaled allergens
This subsample was then augmented with participants who had asthma attacks, experienced shortness of breath at night during the past year, or who were currently taking asthma medications.
The first follow-up examinations for the cohort occurred between 2000 and 2002, and the second was finished by 2013. Data reflecting asthma and hayfever status in children were collected during the second follow-up period.
In total, 5,901 participants were initially recruited to participate in this study. After excluding participants with no offspring, missing information about offspring, or offspring not born between 1972 and 2012, the final sample size was 4,293 participants.
Bertelsen and colleagues estimated adjusted relative risk ratios (aRRRs) to determine the association between parental clinical markers and offspring allergic disease.
When the exposure was parental BHR, the aRRR of offspring developing asthma with hayfever was 2.96 when this exposure was measured before conception, and 1.40 after birth. When the exposure was specific IgEs, the corresponding aRRRs of offspring developing asthma and hayfever together were 3.08 and 1.83, respectively. Of note, all other estimated aRRR values were lower.
These findings were confirmed by performing a sensitivity analysis of a subgroup of children aged 11 to 22 years on which parental disease activity data were available both before and after birth.
“We found that parental BHR and specific IgE positivity measured before conception was more strongly associated with offspring asthma and hayfever than disease activity measured after birth,” the authors wrote. “This was most convincingly shown for mothers’ BHR and mothers’ specific IgE.”
Interestingly, Bertelsen and coauthors noted a gender difference with respect to outcomes.
“When timing of clinical assessment relative to offspring birth was not taken into account, paternal clinical markers of allergic disease appeared to be generally more important than the mother’s clinical markers for offspring allergic disease.”
The researchers suggest that these observed associations are more likely influenced by epigenetic inheritance than either environment or genetics alone. Based on data from animal models and the current study results, Bertelsen and colleagues hypothesize that ongoing respiratory and allergic disease could cause epigenetic changes in parents that are inherited by the next generation. These epigenetic changes then manifest as phenotypic change in children.
This hypothesis has not yet been proven in humans, and further epidemiologic and mechanistic study is needed to confirm. Once these study results are confirmed, the researchers state that it would be important to look into possible treatments and intervention to limit disease risk in of allergies in offspring.
This study was funded by the Ageing Lungs in European Cohorts (ALEC) Study.
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