Trimethylglycine (TMG) for homocysteine reduction
Brecka's approach flips the standard hypertension model: rather than assuming the heart is the problem, he investigates homocysteine as a vasomotor irritant. He recounts Dana White's case—after 25 years of brittle hypertension and four medications, a cardiac ablation was scheduled. Brecka's blood test revealed extremely high homocysteine (low 30s mg/dL, goal <9) and multiple methylation gene mutations. Within 21 weeks on TMG, homocysteine dropped, blood pressure normalized, and all medication was ceased. The head of cardiothoracic surgery at Cedars-Sinai, initially hostile, later apologized and now collaborates with Brecka on complex cases. Brecka generalizes this to 85% of hypertension cases he claims are undiagnosed homocysteine/vascular issues.
Homocysteine is normally recycled to methionine via methionine synthase, which requires methylcobalamin and methylfolate (dependent on MTHFR). When MTHFR is mutated, homocysteine accumulates. TMG acts as a direct methyl donor via betaine-homocysteine methyltransferase, converting homocysteine to methionine without needing MTHFR, thus lowering homocysteine and allowing the vasculature to relax.
Brecka walked Dana White through the protocol personally, coordinated with a physician to taper medications, and received the call when White's blood pressure started dropping too low on meds, signaling success.
I'm going to put you on an amino acid. It's called TMG. It's called trimethylglycine... because you have a gene mutation that impairs this conversion of homocysteine. I'm going to give you an amino acid that skips that gene mutation and allows your body to begin to metabolize homocysteine.

