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Fauziya Naikar: Why the MTHFR Gene is a Critical Piece of the Fertility Puzzle
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May 4, 2026, 06:50

Fauziya Naikar: Why the MTHFR Gene is a Critical Piece of the Fertility Puzzle

Fauziya Naikar, Junior Embryologist at Star IVF and Fertility Center, shared a post on LinkedIn:

“Why the MTHFR Gene is a Critical Piece of the Fertility Puzzle?

​In the embryology lab, we spend our days perfecting morphokinetics and grading.

But beyond the petri dish, a ‘silent architect’ is at work: the MTHFR (Methylenetetrahydrofolate Reductase) gene.

Why do high-quality embryos sometimes fail to result in a live birth?

The answer often lies in the biochemical environment provided by parental genetics—specifically the methylation pathway.

​The Molecular Breakdown.

​The MTHFR enzyme is the critical rate-limiting step in the folate cycle.

Its primary job is to catalyze the conversion of folate into 5-methyltetrahydrofolate (5-MTHF).

This active form is the ‘fuel’ for two vital processes:

  • ​DNA Methylation: This is the cornerstone of epigenetic programming during early cleavage stages. Without it, cellular repair and gene expression are compromised.
  • ​Homocysteine Regulation: MTHFR converts homocysteine into methionine. When mutations like C677T or A1298C occur, enzyme efficiency can drop by 30 percent to 70 percent, causing homocysteine levels to spike.

​The Embryologist’s Perspective: Why It Matters?

We see the effort it takes to create a viable embryo, but that embryo needs a stable environment to thrive post-transfer.

Elevated homocysteine (Hyperhomocysteinemia) is a known risk factor for micro-clots in the placental vasculature (Thrombophilia).

This can lead to:

  • ​Implantation failure or early pregnancy loss.
  • ​Neural tube defects (Spina Bifida, Anencephaly).
  • ​Impaired blood flow to the uterus and placenta.

​Clinical Pivot: From ‘Unexplained’ to ‘Targeted’.

The traditional reliance on synthetic Folic Acid may not be enough for patients with these genetic variants, as their bodies cannot efficiently convert it.

​The Solution?

Bypassing the genetic ‘roadblock’ by using bioavailable Methylfolate (5-MTHF) along with Vitamins B6 and B12.

This targeted approach lowers homocysteine and optimizes the metabolic environment for the embryos we work so hard to cultivate.

​By understanding these genomic markers, we move away from the frustration of ‘unexplained infertility’ and toward a more precise, personalized fertility protocol.

Fauziya Naikar: Why the MTHFR Gene is a Critical Piece of the Fertility Puzzle

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A1298C Anencephaly C677T Fauziya Naikar Fertility Health Hematology Hemostasis News Hemostasis Today Homocysteine Hyperhomocysteinemia Medicine MTHFR Spina Bifida
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