Folic Acid Supplementation and Modifier Dynamics: Is there an Epigenetic Synergy?

Hello everyone!

As a breeder and an enthusiast of Mrs. Stephanie Müller’s methodology here in Brazil, I would like to propose a technical discussion on the interaction between nutrition and genetics.

We know that Dermoid Sinus (DS) is a neural tube defect and that Mrs. Müller’s research has brilliantly mapped how Enhancers and Silencers on Chromosome 18 govern this process. We recognize the Ridge Gene Test 2.0 as the gold standard in this field. However, since genomics provides us with a highly refined statistical probability—rather than absolute phenotypic determinism—there is room to investigate modulating factors.

I would like to raise three points for discussion:

1. Safety Margin: Even in bitches that show high genomic stability (homozygous for protective Enhancers), does it make technical sense to use folic acid as an additional 'safety net'? Or does the stability of these modifiers in such lineages make nutritional intervention irrelevant for this specific purpose?
2. Ridge Expression vs. Silencers: Mrs. Müller’s paper presents the fascinating case of dogs that carry the Ridge gene (R/r) but are phenotypically ridgeless due to the action of silencers. If the visibility of the ridge depends on Enhancers overcoming Silencers, is there any evidence that folate support could aid in proper expression during embryogenesis?
3. Epigenetic Modulation: In matings where genomic modeling indicates a higher probability of instability, could folic acid act as a modulator (methyl group donor) to help 'silence' potential failures, or is the mapped genetic load too dominant to be influenced by external factors?

I would love to hear the thoughts of Mrs. Stephanie and other breeders regarding B9 protocols.

Best regards from Brazil!