5-Amino-1MQ and NNMT inhibition: hype vs. what studies show

What did @drtrevorbachmeyer actually say?

The video argues that an enzyme called NNMT is actively destroying your NAD+ precursors and methyl donors, and that 5-amino-1MQ, a selective NNMT inhibitor, fixes this by rerouting nicotinamide into NAD+ production. The claims escalate quickly. By the end, 5-amino-1MQ is being connected to obesity reversal, insulin resistance, and cancer cell death in glioblastoma and pancreatic tumors.

The specific numbers are bold: "a 47% reduction in fat mass" from a 2017 Nature paper, insulin resistance reversed "no diet, no exercise" from a 2018 Molecular Metabolism study, and NNMT cited as a "key metabolic dependency for pancreatic cancer stem cells" from a 2020 Nature Communications paper. He also says cancer cells "over-express NNMT" and that 5-amino-1MQ triggers "apoptosis" in them specifically. The throughline is that blocking NNMT is a metabolic master key.

Does the science back this up?

Partially, and the gap between what the studies actually showed and what this video implies is significant. The core biochemistry is real. NNMT does consume nicotinamide and SAM, and inhibiting it does increase NAD+ precursor availability. But every study cited was conducted in mice or cell cultures, not humans. That distinction matters enormously.

The 2017 Nature paper (Kraus et al., Nature) did show fat mass reductions in diet-induced obese mice treated with an NNMT inhibitor. The effect was real in that model. The 2018 Molecular Metabolism study (Kannt et al.) also demonstrated improved insulin sensitivity in rodent models. The 2020 Nature Communications paper (Broadfield et al.) on pancreatic cancer stem cells is legitimate research, but it was conducted in cell lines and mouse xenograft models. No clinical trial in humans has demonstrated that 5-amino-1MQ does any of these things in a living person. Saying "nearly half their body fat gone" without specifying this was in mice is a material omission that changes everything.

What did they get wrong (or right)?

They got the mechanism directionally right. NNMT does sit at the intersection of NAD+ metabolism and methylation, and the enzyme is genuinely overexpressed in several cancers and in adipose tissue of obese individuals. That part is textbook biochemistry supported by peer-reviewed literature. Credit where it is due.

What they got wrong is the leap from mouse data to human outcome framing. Describing "47% reduction in fat mass" without the word "mice" is not a minor oversight. It is the kind of framing that leads people to believe a compound has proven human efficacy it simply does not have yet. The cancer section is the most problematic. Saying 5-amino-1MQ "triggers apoptosis" in cancer cells and framing it as "giving good cells a weapon" while "exposing bad cells' flaws" implies a therapeutic effect in humans that no clinical evidence supports. The statement that "type two diabetes is not a blood sugar problem, it's a cellular deafness problem" is reductive to the point of being misleading, though the insulin signaling angle is a real area of research. Calling NAD+ "the cofactor for life itself" is marketing language, not science.

What should you actually know?

5-amino-1MQ is not FDA-approved. It is not a peptide; it is a small molecule compound. It is available through some compounding pharmacies and research chemical suppliers, but it has no completed Phase I, II, or III clinical trial data in humans as of mid-2025. That means no established safety profile, no confirmed effective dose, and no regulatory oversight of quality or purity.

The underlying research is genuinely interesting. NNMT inhibition as a metabolic strategy is being actively studied, and the preclinical data across obesity, metabolic disease, and oncology is promising enough to justify continued investigation. But promising preclinical data has a poor track record of translating into human outcomes, and that history deserves weight. If you are considering 5-amino-1MQ because of content like this, the honest conversation starts with what is not known, not what mice experienced in a controlled lab setting. Talk to a clinician who can review your metabolic labs and assess whether any intervention in this space is appropriate for your situation.