HFE Iron SNPs and Lyme Disease.....who knew?
I recently participated in a Lyme Study with MethylGenetic Nutrition AnalysisTM. The data collected indicated that specific genetic variants are common in those with chronic Lyme Disease and/or chronic illness! We examined over 350 genes that are involved with mitochondria function, methylation, neurotransmitter production, antioxidant production and patterns what may result in excess production of oxidative stress, including superoxide, glutamate, ammonia and peroxynitrite. The results were fascinating and give us the knowledge necessary to help those suffering from illnesses due to these genetic variant patterns.
The HFE SNPs are known for their association with higher levels of iron absorption and hemochromatosis and appear to be critically important in their relationship to Lyme Disease and/or chronic illness. The HFE gene provides instructions for producing a protein that is located on the surface of cells, primarily liver and intestinal cells. The HFE protein regulates the production of another protein called ‘hepcidin,’ which is considered the ‘master’ iron regulatory hormone.
An iron overload condition in which mutations of certain genes involved in iron metabolism, disrupt the body’s ability to regulate the uptake of iron, causing increased intestinal iron absorption. The most common form is caused by mutations in the HFE gene, which are inherited recessively and commonly found in people with European ancestry. If you have any suspicion that you may have the hemochromatosis genes, please go to your doctor and get a simple blood test.
Increased body stores of iron in various clinical situations may tip the immune system regulatory balance unfavorably to allow increased growth rates of infectious organisms, and complicate the clinical management of pre-existing acute and chronic diseases! Wow, that’s worth reading again, it’s very important!
As a chemical component of heme in hemoglobin, iron is capable of carrying oxygen throughout the body. Behaving in this way, iron is a life saver. However, 'free' or unbound iron can contribute to the development of free radicals. Unbound iron contributes to creating free radicals, leads to liver disease, pancreatic 'burn-out' (Type II Diabetes), joint disease, heart disease, neurological problems and exacerbates aging. It's purely anecdotal, but rarely do you see cases of pancreatic cancer in people without iron issues or the HFE SNPs. www.irondisorders.org
Further research is needed to determine if iron oxidation from the 
Fenton Reaction is a contributing factor to those with Chronic Lyme, and if nutritional interventions with nutrients that may slow iron absorption, regulate iron, support cysteine to glutathione and superoxide dismutase, may be an appropriate holistic approach.
A combination of HFE SNPs along with other specific SNPs create a potential for hydroxyl radical production SNPs. For example, CBS699 and BHMT-08 may increase the cysteine, while the glutathione variants may slow the conversion of cysteine in to glutathione. Variants in SOD genes may slow the ability to neutralize the hydroxyl radicals. Thus, we have too many hydroxyl radicals that create more inflammation, lower our immune function and this adds to our toxic burden.
Let's find out what's going on with your SNPs. To learn more about your genetic makeup and how it influences your health and longevity, sign up for a 'Comprehensive Nutrigenomic Consultation.'
