Gold Beads Implantation (GBI) – The Scientific Basis
Dr. Sagiv Ben-Yakir BSc(Biology), DVM(in honor), MRCVS,
CVA(IVAS), CVHomotox(Baden-Baden, Germany)
Received: January 2009
Noble metals, like gold, have been used since ancient times
as cures for a wide range of diseases (1). The use of gold implants was
originated from acupuncture where gold needles had been used in the Far East (1).
In the early 1970s some American veterinarians (Dr. Grady
Young, followed by Dr. Terry Durkes) started to treat dogs suffering from hip
dysplasia with gold implants (2). The implantation was usually done at acupoints
GB-29, GB-30, and BL-54, which lie close to the affected hip joint. Other
arthritic conditions (e.g. elbow arthrosis, spinal spondylosis etc) had been
treated similarly by implanting gold beads in other local acupuncture points
chosen accordingly (3). Today, many veterinary acupuncturists around the world
implant gold beads, or short lengths of 24-carat gold wire, routinely to treat
chronic diseases in animals.
The mechanism of action proposed by proponents of gold beads
implantation (GBI) is that the gold implants emit a minute positive electrical
charge that neutralizes a negative electrical charge of the point, producing
analgesia and preventing further arthritic changes at the joint
However, there is another possible explanation for the basic
scientific mechanism behind GBI. On insertion of metallic gold beads, in vivo
and in situ, it was found that gold ions are released from the implanted gold
and diffuse out into the surrounding tissue. This phenomenon mimics on a local
scale the treatment with gold-containing drugs used for arthritic conditions
Almost immediately after implantation, local macrophages and
other inflammatory cells attach themselves to the metallic gold surfaces (6).
This attachment is mediated by activation of the complement system as C3 adsorbs
to the implant surface. The C3 forms complexes with complement factor B or
factor H resulting in the formation of C3b or iC3B respectively. C3b or iC3B are
both ligands for macrophages surface receptors. Additionally, fibronectin and
vitronectin also absorb to the locally implanted surface of the gold bead and
act as a ligand for the macrophages through RGD-integrin receptor domains. These
and other ligand-interactions are the primarily interactions between gold
surface and macrophages and other inflammatory cells. The inflammatory cells
produce an ultra-thin layer, a dissolution membrane, within which the necessary
chemistry for liberation of gold ions is found. This is 10-100 nm thick biolayer
membrane essential for the dissolution of metal implants and particles (which
cannot be phagocytosed).
The inflammatory cells (e.g. macrophages, other neutrophils)
release cyanide into the dissolution membrane and into their immediate
surroundings (7,8,9). The following chemical process occurs:
4Au + 8CN- + 2H20 + O2 = 4[Au(CN)2]- + 4OH-
The complex ion aurocynide Au(CN)2- , a relatively stable
ion, inhibits the lysosomal enzymes of inflammatory cells in the synovial tissue
and decreases the number of inflammatory cells in situ. Also, the aurocynide
ions inhibit antigen processing and suppress NF-kappa B-binding activity and
I-kappa B-kinase activation, and in turn reduce the production of
pro-inflammatory cytokines. Aurocynide is the active substance that inhibits the
cellular functions of inflammatory cells (10,11,12).
Also, these ions move from their dissolution membrane
location into intercellular space, where they are taken up both by the
macrophages and by other inflammatory cells further away.
It was found also that the longer the gold implant stays in
the inflamed tissue, the further away gold ions are carried by inflammatory
cells. It was also found that when the cells surrounding the gold implant become
heavily loaded they leave their position on the dissolution membrane and are
replaced by new inflammatory cells (5,6).
1. “Gold Symposium 1st, June 20, 2007 at Institute of Anatomy, Aarhus University Denmark.
2. “Gold Bead Implants” by Durkes T. E. in “Veterinary Acupuncture, Ancient Art to Modern Medicine” ed. by
Schoen A. M. 2nd edition, Mosby, USA, 2001, Chapter 25, pp 303-305.
3. “Gold Bead Implantation” by Durkes T. E. in International
Veterinary Acupuncture Society Certification Course notes, San Diego, USA,
4. “Revolutionary new pain theory and acupuncture treatment
procedure based on new theory of acupuncture mechanism” by Takase K, in Am J.
Acupuncture 11:305-323, 1983.
5. “In vivo liberation of gold ions from gold implants. Autometallographic tracing of gold in cells adjacent to metallic gold”
by Danscher G. in Histochem Cell Biol 117:447-452, 2002.
6. “In vitro liberation of charged gold atoms: autometallographic tracing of gold ions released by
macrophages grown on metallic gold surfaces” by Larsen A. Stoltenberg M and
Danscher G in Histochem Cell Biol 128:1-6, 2007.
7. “The activation of gold complexes by cyanide produced by
polymorphonuclear leukocytes, the formation of aurocynide by myeloperoxidase” by
Graham G.G in Biochem Pharmacol 39:1697-1702, 1990.
8. “Serum lysozyme: a potential marker of monocyte/macrophage activity in rheumatoid arthritis” by Torsteindottir I et al in Rheumatology
9. “Molecular mechanism of action of gold treatment in rheumatoid arthritis: an update” by Burmester GR
in Z. Rheumatol 60:167-173, 2001.
10. “Mechanism of action of disease modifying anti-rheumatic agent, gold sodium thiomalate” by Mangalam A. K. in Int
Immunopharmacol 1:1165-1172, 2001.
11. “Inhibition of IL-6 and IL-8 induction from cultured rheumatoid synovial fibroblasts by treatment with aurothioglucose” by
Yoshida S et al in Int Immuno 11:151-158, 1999.
12. “Inhibition of the DNA-binding activity of NF-kappa by gold compounds in vitro” by Yang J.P. in FEBS Lett 361:89-96,