Counterpoint: An alternative hypothesis for why exposure to static magnetic and electric fields treats type 2 diabetes

We thank Petersen et al. (1) for their comments and interest in our work. Based on the evidence gathered to date, we continue to highly favor the redox hypothesis over the alternative hypothesis for the reasons stated in our initial response above.

We invite interested individuals to read our published manuscript (2). We suggest consideration of the following: 1) the difference in strength and character of the static magnetic and static electric (sBE) fields (2) compared with the fields upon which the alternative hypothesis is based (3) (500× stronger than sBE); 2) the data described in our initial response that directly contrasts with what is predicted by the alternative hypothesis, including unchanged glucose uptake into muscle, increased hepatic glycogen, and no evidence for activation of the sympathoadrenal response or adrenocortical activation with sBE exposure; 3) our findings that modulating the homeostasis of mitochondrial reactive oxygen species (ROS) moieties specifically in the liver fully abolishes the insulin sensitizing effects of sBE (2); 4) our findings that modulating the systemic redox environment rapidly alters insulin sensitivity (2), which is consistent with prior studies that have demonstrated that the extracellular redox environment regulates insulin sensitivity (4–7); and 5) our findings that sBE exerts biological effects in vitro on primary hepatocytes, which lack a vestibular system.

Together, these points lead us to conclude that sBE exposure modulates the insulin response independently of the vestibular system.

Although much remains to be discovered about the complete mechanism, based on our data to date, we propose that sBE exerts biological effects via interactions with hepatic mitochondrial ROS and the systemic redox environment. Additional studies are underway to better understand the remarkable metabolic effects of sBE exposure in the context of type 2 diabetes, as well as other redox-related diseases. We look forward to sharing new and exciting findings in future publications.

DISCLOSURES

C.S. Carter, S.C. Huang, V.C. Sheffield, C.C. Searby, and M.J. Miller have patents pending related to this work. C.S. Carter, S.C. Huang, and W.A. Carter are founders of Geminii, Inc. D.R. Spitz has a sponsored research agreement with Galera Therapeutics.

AUTHOR CONTRIBUTIONS

C.S.C., S.C.H., and V.C.S. drafted manuscript; S.C.H., E.B.T., A.W.N., G.R.B., J.M.H., D.R.S., and E.D.A. edited and revised manuscript; C.S.C., S.C.H., B.C., M.J.M., W.J.G., T.B.P., T.K.P., S.A.W., M.A., Q.Z., K.A.M., G.L.M., A.O.H., D.-F.G., R.W., K.B., E.B.T., A.J.R., D.W.D., V.A., K.C.F.-H., B.A.W., W.A.C., K.W., A.W.N., K.R., G.R.B., J.M.H., D.R.S., E.D.A., and V.C.S. approved final version of manuscript.