Assessing epigenetic origins of allergies and asthma

This 2015 German paper described the study design of a birth cohort that’s being established to:

“Assess potential associations between early-life exposures and onset of childhood asthma and allergies taking into account epigenetics.

The study builds upon an existing cohort which has been recruited [1995] and in the meantime has been followed up twice [2002 and 2007].

This approach provides the unique opportunity to assess the effects of genetic predisposition, epigenetic factors, and environmental factors such as exposure to environmental tobacco smoke, living conditions, and parental occupation in a prospective and cross-generational study.”

The paper had informative references, one of which was the 2013 Epigenetic mechanisms and models in the origins of asthma:

“We need to determine whether epigenetics should be considered as a major integrator of multiple signals, or, alternatively, whether DNA methylation acts differently at various developmental stages conditional on genetic variants and exposures.

In addition, since there is a lack of critical knowledge on which genes are programmed or re-programmed at what time during gestation and in which developmental phase, birth cohort studies need to trace DNA methylation over time, and ideally over generations.

This will provide critical information about which phases in the course of life are most suitable to prevent deviant DNA methylation (preventive epigenomics) or intervene to normalize DNA methylation to prevent disease (pharmaco-epigenomics).” “Establishing a birth cohort to investigate the course and aetiology of asthma and allergies across three generations – rationale, design, and methods of the ACROSSOLAR study”

I was encouraged by the referenced review’s emphasis that researchers start their investigations at the beginning of human life for causes that produce later-life effects. Subsequent emphasis on prevention was commendable.

The review also revealed a prevalent researcher bias, that causal and curative results of human disease will be found on the molecular level rather than in human experiences. This preconception leads to ignoring human elements that generate epigenetic changes that manifest themselves in symptoms such as asthma and allergies.

I don’t know how including human emotions in studies became viewed as unscientific, but here we are. I didn’t see any indication that its study design included investigating emotional states other than possibly work-related stress.

These researchers will have to pretend that proven etiologic factors such as emotional states of a pregnant woman have no affect on nervous and immune system development of her fetus. These human elements are unjustified exclusions from a study designed in 2015, but they’re easily ignored when they aren’t measured.

Here’s a search of what Dr. Arthur Janov had to say about allergies over the past eight years. A representative sample from earlier this month was:

“Every therapy we try will be temporary, something we need to do over and over again. It can be nothing else because the imprint has the force of survival, of a lifesaving memory and must endure until the life-endangering imprint is finally fully felt and resolved.

Clearly this applies to many problems, from high blood pressure to asthma and allergies. That is why it is urgent that we re-focus on the real problem.”

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