What is MTHFR and why should you care when you have Hashimoto’s hypothyroidism or brain issues?11/14/2019
Have you been googling for ways to improve your hypothyroid or brain condition and come across suggestions to test MTHFR? What is MTHFR and what does it have to do with hypothyroidism or the brain? If you are one of the 60 percent of people with a genetic defect in the MTHFR gene, it could affect your ability to successfully manage Hashimoto’s hypothyroidism or brain-based symptoms.
MTHFR is the acronym for methylenetetrahydrofolate reductase, an enzyme involved in processing folate, or vitamin B9, into a usable form the body can assimilate. It’s also necessary to metabolize folic acid, a synthetic form of folate used in supplements. Thanks to the popularity of gene testing, people can now learn whether they have a mutation in the MTHFR gene. If so, it means their methylation pathways are impacted and contributing to health challenges. Methylation pathways govern detoxification and many important metabolic processes in the body, which makes a MTHFR defect something worth paying attention to. If you are struggling to manage your Hashimoto's hypothyroidism or brain-based symptoms such as brain fog, fatigue, or depression, you may find the MTHFR test valuable. Methylation is a process of adding a methyl group to a molecule. Methylation’s roles jobs include the following:
Proper methylation means one can efficiently make proteins, use antioxidants, metabolize hormones, enjoy more balanced brain chemistry, detoxify toxins and heavy metals, and dampen inflammation. All of these factors are vital to managing Hashimoto's hypothyroidism and brain-based symptoms. However, if you’re one of the 60 percent of people with a MTHFR genetic defect, you may not be able to properly break down folate in foods or folic acid in supplements. An inability to properly process folate can raise levels of homocysteine. Homocysteine is an amino acid in the bloodstream that can be dangerous when levels are too high. High homocysteine is linked to an elevated risk of heart disease and Alzheimer’s. Poor methylation also impacts another vital process — the production of glutathione, the body’s main antioxidant. When we become deficient in glutathione, we lose our natural defenses and are at higher risk of developing autoimmune diseases, food sensitivities, and chemical sensitivities. An MTHFR defect can also impair the body’s ability to synthesize important brain neurotransmitters, so that brain-based disorders may arise. An MTHFR defect has been linked to depression, anxiety, brain fog, ADHD, bipolar disorder, and even schizophrenia. Because methylation is involved in so many important processes in the body, an MTHFR gene defect has been associated with many health conditions, including:
If you are trying to manage a condition like Hashimoto's hypothyroidism or brain-based symptoms, it’s imperative that you be able to dampen inflammation and raise glutathione levels. An MTHFR defect can work against you. Fortunately, it can be easy to address. First of all, you can test for MTHFR gene mutations through genetic testing companies such as Spectracell or 23andme.com, and get an interpretation at geneticgenie.org. More than 50 MTHFR genetic mutations exist, but the two considered the most problematic are C677T and A1298C (written as just 677 and 1298). Also, keep in mind gene defects don’t always become activated. If you show those genes on a test it doesn’t necessarily mean they have been expressed and are causing symptoms. To address a MTHFR enzyme defect, support your methylation pathways with methylfolate and methylcobalamin (methyl B12). Avoid supplements with folic acid, boost your glutathione levels with high quality oral liposomal glutathione, and minimize your exposure to toxins. These are also beneficial strategies to aid in the management of Hashimoto's hypothyroidism and brain-based symptoms. Ask my office for more advice on managing autoimmunity or brain inflammation. Should you have any health questions please call the office at 317-848-60 Comments are closed.
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