This summary was compiled from the tweets posted by allergists/immunologists who attended the 2013 annual meeting of the American Academy of Allergy Asthma and Immunology (AAAAI) (see the list at the end). The tweets were labeled #AAAAI. The text was edited and modified by me.
Early life environmental influences on development in allergic diseases
Susan Prescott MD PhD (@susanprescott88) presented on early life environmental influences on development in allergic diseases
Allergic disease is the most common, and the earliest onset, non-communicable disease. Non-communicable diseases (NCD) are more common in affluent and industrialized nations, but ironically burden the poor the most. Despite the prevalence of allergic disease, it has largely been neglected on the world political stage, when compared to other NCD's.
By 2030, expect 52 million deaths from NCD's. This crisis can't be addressed without combatting factors which dictate our risk. Big 4 NCDs - Type 2 DM, COPD, heart disease and cancer. Inflammation is a common feature of all NCDs (non communicable disease).
Dr Prescott: We live a life similar to animals in captivity, so we shouldn't be surprised when we have stress levels similar to them.
Jonathan Tam @sirartichoke: Irony: Dr. Prescott warns of the dangers of sedentary indoor lives to dark room full of sitting allergists with full day of lectures planned.
"There are no areas in the world where food allergy is declining"
In Australia 16% of children had sensitization to egg and half had a positive challenge. Highest in the world. People of Asian genetic background appear to have a higher propensity to atopy/food allergy, especially in Westernized countries.
There is an Interdisciplinary, international network studying inflammatory diseases: In-FLAME.
Early life inflammation leads to increased C-reactive protein (CRP) during pregnancy and early life associated with inflammatory disease. In utero exposures may drive predisposition to sustained inflammatory responses.
Affluence --> Low microbial environments --> increased baseline inflammation --> sustained inflammatory response --> increased Non-communicable diseases (NCD).
Allergy itself further drives ongoing inflammation and can increase risk of other NCD's, e.g. cardiovascular disease.
Biodiversity in GI tract may be protective
Has eradicating H. pylori increased risk of obesity, insulin resistance, autoimmunity, allergy, asthma? Modern diets alter the gastrointestinal microbiome, thus increasing risk of NCD. Can pre/probiotics help modulate this risk?
Antibiotics from agricultural products (even low doses) can alter human gut flora and increase risk of metabolic disease.
Smoking and pollutants, diet, microbial exposures can also modulate gene expression. There are incredibly intertwined relationship of genetics and environment.
What can we do to induce tolerance in early life?
Exercise, stress-reduction during pregnancy, low-inflammatory diet, microbial biodiversity are all potential measures.
A BMJ fish oil study in pregnant women showed a small but stat significant reduction in AD and egg allergy.
A Cochrane review of the use of probiotics for allergic disease showed improvement in atopic dermatitis but no other allergic disease.
Harald Renz presented on gene-environment interaction in chronic inflammatory disease.
Pre- and post-natal environment provides an opportunity for early immuno-education and programming. Having older siblings, early day care, traditional farming lifestyle are all associated with lower risk of asthma.
Acinetobacter lowfii, Staph sciuri, Lactococcus lactis, Lactobacillus GG, and others may reduce asthma risk.
The microbial "fingerprint" is unique in various organ systems. Intestinal and pulmonary microbiomes are linked.
C-section is associated with a different microbiome for baby than vaginal delivery. It is associated with increased risk of asthma, atopy. Someone in audience mentioned they're aware of study where children born by C/S and having their Mom's vaginal secretions given to them.
In each cell, only about 20K of 100K genes will actually be expressed - determined by chromatin packaging. If the chromatin is packaged in the "wrong way", celles will get aberrant gene expression that lead to disease states in those cells. If chromatin is heavily condensed you won't see gene expression - histones and methyl groups influence this.
We used to think that 98% of genome is "junk" DNA - we now know this junk DNA contains important determinants of gene expression. Epigenetics can explain population changes over time that would not be explained by things like Darwinian theory.
Genome is static; Epigenetic is dynamic - subject to continuous "editing"
We were all born with a genetic "script" that can be modified with environmental exposures - can edit our script. Developmental plasticity may explain early origins of human disease such as allergy and asthma. Exposure to synthetic chemicals, pollutants and dietary choices can influence disease development via epigenetic alterations.
Maternal exposure to polycyclic aromatic hydrocarbons was associated with childhood wheeze in Ho's study through gene hypermethylation. We need to think about exposures as groups not just individually - Ho calls this an "Exposisome".
Firefighters are examined because of frequent chemical exposures. They've studied a gene that gets modified the longer they work.
There are several ways through which epigenetics works to affect gene expression - non coding RNAs, DNA methylation, histone acetylation or modification. DNA methylation leads to gene silencing. Prenatal tobacco smoke exposure affects global and gene specific DNA methylation.
Hypomethylation increases with age - "Epigenetic Drift".
Biome and Immune Interactions
Andrew Kau presented on sorting out microbiota, diet and immune interactions: lessons from malnutrition.
Human microbiota: we are all living with a large variety of microorganisms. Skin, gut, sinopulmonary tract, etc. Nutritional value of food is shaped by microbiota.
16S rRNA gene is characterized as powerful method of classifying different bacteria, using PCR amplification.
Enterobactericeae colonization in small intestine is associated with environmental enteropathy. Akkermansia muciniphilia is a microbe which may be protective against inflammatory bowel disease.
Jeffrey Gordon, MD presented on Microbiome in Health and Disease. The Gordon Lab URL: http://gordonlab.wustl.edu
The Gut Microbiome is like “Dining with Trillions of Fascinating Friends.”
Microbiota = collection of microorganisms. Microbiome = collection of genes present in the microbiota.
Our microbiota varies as a function of lifestyle. Therefore, it can only be understood in the context in which we live. By mid-century, world population will be ~9 billion. How can we feed all these people in a healthy way? Can studying the gut microbiome help us identify which foods are compatible with long-term health?
We begin to develop microbial colonization at birth, and it transitions to the "adult" pattern in the first 3 years of life.
In industrialized societies, there is less biodiversity within the gut microbiome than in agrarian societies.
Maternal vitamin D and asthma risk
Maria Magnus presented on maternal vitamin D and asthma risk.
1,25-dihydroxy vitamin D is the active form of Vitamin D. Maternal 25(OH)D increased with age and education, and varied by month of sampling. There was an inverse association between maternal vitamin D and asthma/LRTI in children.
Use of forced air HVAC and incidence of asthma trend up together. VOC's are more predominant indoors, as houses are built to be so airtight nowadays. Tighter homes estimated to increase asthma symptoms by 20%.
Damp indoor spaces are a major risk factor due to dust mite, mold and pests. Mold in damp environments is associated with the development and severity of asthma.
Installation of insulated windows is associated with increased levels of house dust mite.
Bisphenol A (BPA)
BPA is found in most types of plastics and is an estrogen mimetic and 93% of Americans have detectable urinary BPA.
BPA (bisphenol A) may increase risk of CAD, brain tumor, miscarriage, PCOS. Approximately 90% of population is exposed.
"BPA-free" generally means that Bisphenol S (BPS) has been substituted. Some studies suggest BPS may be even worse than BPA.
Allergists are on Twitter - follow them
Allergists increased Twitter use 470% in one year - 25 allergists reached 250,000 individuals from the 2012 #AAAAI meeting (see the references here). This summary was compiled from some of the tweets posted by the following allergists:
This is a list of the allergists who used Twitter to post updates from the 2013 #AAAAI meeting. The list is open for edit, please feel free to add your own info.
I would strongly encourage you to post updates on Twitter from the CME conferences that you are planning to attend in the future. Here is how to do it: Twitter for Physicians: How to use Twitter to keep track of the latest news and scientific meetings, and share information with colleagues and patients.
Disclaimer: The text was edited, modified, and added to by me. This is one of a series of posts that will be published during the next few weeks.
Comments from Twitter:
Dr John Weiner @AllergyNet: Good info here. Thank you MT @Allergy: Microbiome and Allergy - Twitter summary from 2013 #AAAAI meeting bit.ly/WwOzf9
Airmid Healthgroup @AirmidHealth: Twitter summary 2013 #AAAAI via @Allergy Mold in damp environments associated with asthma development & severity goo.gl/fb/2FQd8