The Overlooked Link Between MTHFR Mutations, Hyperhomocysteinemia, PCOS, Fibromyalgia, Chronic Inflammation, and Renal Decline — and Why Precision Genetic Testing May Be the Missing Step
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This is a clip from https://danpursermd.substack.com/p/high-homocysteine-mthfr-mutations?utm_source=youtube_shorts
See the full video: https://www.youtube.com/watch?v=HuQbQ1IqNIM
#shorts #substack
High homocysteine often shows up first as widespread inflammation—pain all over, poor circulation, or even early warning signs of cardiovascular problems like stroke and heart attack. The best way to know for sure is through testing: a blood test can measure homocysteine directly, while a CMA with Redox uncovers the vitamin deficiencies driving it. For genetic causes, the DRP Genetics panel screens 15–16 of the 17 known SNPs that can cause permanently high homocysteine. If your levels are fixed by genetics, reduced glutathione and targeted B vitamins (like MTHFR Daily) are key to balancing the
High homocysteine levels can lead to inflammation, joint and muscle pain, and even shifting pain throughout the body. It’s also linked to birth defects and chronic kidney failure, and can raise blood pressure. Six genetic SNPs (like MTR, MTRR, and CBS) and MTHFR mutations (like C677T) can prevent homocysteine from converting into glutathione, which is essential for keeping inflammation in check. Plus, 12 vitamin deficiencies may temporarily raise homocysteine levels, so addressing these deficiencies is key.
Your body’s ability to detox depends on one critical pathway—turning homocysteine into glutathione. But for millions with MTHFR or other genetic SNPs, this process is broken, leaving them vulnerable to toxins, inflammation, and cytokine sto
🚨 High homocysteine isn’t just a lab number—it’s a warning sign.
Genes like MTHFR, MTR, MTRR, and GGH can overactivate the methylation cycle and lead to hyperhomocysteinemia, which drives inflammation, stroke risk, and even kidney failure.
Homocysteine levels can persistently be elevated if you possess any of seven genetic Single Nucleotide Polymorphisms (SNPs), such as MTHFR, CBS, or FOLH1. When these genes are homozygous, they disrupt the transulfuration pathway, resulting
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