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Research

1. Morley Robbins

  • Main speaker and expert.

  • Founder of the Root Cause Protocol and the Magnesium Advocacy Group.

  • Central figure explaining the role of the PAM enzyme, copper metabolism, and associated biochemistry.


2. Richard Mains

  • Researcher mentioned repeatedly for pioneering work on the PAM enzyme.

  • Conducted significant research with Dr. Betty Eipper at Johns Hopkins and later at the University of Connecticut Medical Center (UConn).

  • Studied defects in the PAM gene and the effect of copper deficiency on PAM expression in animal models.

  • Demonstrated that copper supplementation could restore PAM activity.


3. Betty Eipper

  • Researcher, wife and scientific collaborator of Richard Mains.

  • Co-led research on PAM enzyme, copper metabolism, and peptide activation.

  • Key figure in advancing knowledge on how copper deficiency impacts neuropeptides.


4. Leslie M. Klevay

  • Longtime copper researcher, still publishing into his late 80s/90s.

  • Authored the article “Chronic Copper Deficiency” (2022).

  • Also published a 1986 paper linking copper deficiency and hyperglycemia.

  • Cited a 1981 pediatric textbook noting that children with Menkes disease are the most glucose-intolerant population—supporting copper’s vital role in sugar regulation.


5. Joseph Prohaska

  • Copper researcher active in the 1980s–1990s.

  • Referenced for work on intracellular copper status, especially in red blood cells.

  • Studied markers like superoxide dismutase (SOD) and CCS (copper chaperone for SOD)to detect copper deficiency.

  • Highlighted how in deficiency, SOD is low, but CCS is high, indicating the body is “looking” for copper.


6. Sternlieb and Scheinberg

  • Researchers from 1960, working at ATT Labs in Upstate New York.

  • Developed the Copper-to-Ceruloplasmin Ratio of 3.33:1, considered ideal for bioavailable copper function.

  • Their work serves as a foundational principle in Morley Robbins’ copper analysis today.


7. Myra Fields

  • Researcher cited for work in the 1980s and 1990s.

  • Demonstrated that fructose blocks CTR1, the copper transporter protein (the “front door” for copper entry into cells).

  • Her research supports the idea that dietary fructose impairs copper absorption, leading to widespread deficiency.

Copper is a Redox-Active Metal

Its primary roles include:

  • Electron transfer: Cytochrome C Oxidase CCO.
  • Reactive oxygen species ROS control: Superoxide Dismutase SOD.
  • Extra Cellular Matrix ECM structure: Lysyl Oxidase LOX.
  • Copper is normally bound to:
  • Ceruloplasmin: systemic transport + redox buffering.
  • Metallothioneins: intracellular buffering
  • Enzymes: functional copper.

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