MTHFR as Purposeful Slowdown
What if your "broken" methylation is actually protecting you?
The Conventional View
You have an MTHFR variant. Your methylation is reduced by 35-70%. The standard advice: supplement with methylfolate to "fix" it. Push that methylation back up to where it "should" be.
But what if this advice is backwards?
The Longevity Paradox
The MTHFR T allele appears more frequently in people aged 90 and older. If it were purely harmful, it should disappear with age.
The TT genotype (homozygous variant) shows a 32% reduced risk of prostate cancer. The "dysfunction" provides protection.
The Theory: Protection Through Slowdown
Methylation isn't free. Every time your body methylates something, it generates oxidative stress through the SAM-ubiquinone pathway. More methylation = more reactive oxygen species = more cellular damage.
MTHFR variants slow this process down. Less methylation means less oxidative stress, less mitochondrial damage, and potentially longer life. The body may be trading short-term capacity for long-term protection.
This explains why methionine restriction (which also reduces methylation) extends lifespan by up to 45% in animal studies. It's not despite the reduced methylation. It's because of it.
The Tradeoff
High Methylation Provides
- Better DNA synthesis and repair
- Normal homocysteine levels
- Proper neurotransmitter methylation
- Adequate gene expression regulation
High Methylation Costs
- Higher mitochondrial ROS production
- More oxidative damage to proteins and DNA
- Accelerated aging markers
- Depleted glutathione reserves
Context determines which side of this equation matters more for you.
When Slowdown Protects
The Implication
Rather than asking "How do I fix my MTHFR?" the better question might be: "What is my body protecting me from?"
For someone with high oxidative stress, pushing methylation "to fix the genetics" may actually override a protective mechanism. The variant isn't the problem. It's the messenger.