Curtis Eckhert

Dr. Eckhert is a world expert on dietary trace elements having authored the chapter on Trace Elements in the last three editions of Modern Nutrition in Health and Disease a highly recognized reference and the major text in graduate nutrition education. His current focus is on boron an element that humans absorb from diet in the amount of about 1 mg/day. Boron was discovered to be essential for plants for nearly 70 years before researchers were able to isolate its effects from other nutrients in animal diets.  The Institute of Medicine lists it as beneficial for humans, but very little was known about its function or whether it was essential in animals. Dr. Eckhert performed a critical study in this effort showing that boron was essential for the cleavage of a zebrafish fertilized egg (zygote) into two and then four cells.  This occurs before the onset of embryonic gene expression and proved boron was essential to moving from one generation to another.  His laboratory then developed procedures to deplete boron in yeast and mammalian cells setting up conditions to learn what boric acid (BA), the form present in physiological fluids, was doing at the molecular cell level.  To identify a dietary boron responsive health effect in humans Dr. Eckhert collaborated with Dr. Zhang, a cancer epidemiologist.  Using the methods of epidemiology as a screening tool they found dietary boron was associated with a reduced risk of prostate cancer in a dose dependent manner.  A similar reduction in risk was shown across a boron groundwater gradient in Texas providing support for the hypothesis that boron was chemopreventative.  These observations stimulated others into the field and boron was quickly shown to be protective against cervical dysplasia, lung cancer and enlargement of the prostate.  The Eckhert lab’s approach to identify the underlying mechanism of boron chemoprevention used mass spectrometry to identify and characterize molecular targets of BA, confocal imaging to identify functional molecular targets in live cells, and molecular biological techniques to tease out the downstream molecular pathways leading to cancer prevention.  His lab demonstrated cyclic ADP ribose (cADPR) binds boric acid and physiological concentrations BA act as a reversible competitive inhibitor of cADPR function the only known endogenous agonist of the ER ryanodine receptor Ca2+ channel.  Boric acid treatment lowers Ca2+ stores in the endoplasmic reticulum (ER) which serves as an intracellular signal that causes changes in mRNA expression and gene products to protect the cell from stress.  The effect is rapid and measurable after only 15 minutes post-treatment which is consistent with the rapid response observed in the early zebrafish studies.  Subsequent studies identified the sequential activation of molecular pathways that activate naturals antioxidant genes and protect against DNA damage.  This provided a proof of the principal that changes in BA levels in serum that can be achieved by diet are sufficient to activate molecular pathways within a timeframe that can protect cells from toxic substances consumed in the diet.    

Dr. Eckhert received his Ph.D. in biochemistry and nutrition from Cornell University (1974). Thereafter he conducted postdoctoral research in neurochemistry (Cornell), trace element metabolism (UC Davis) and visual biochemistry (Stanford). He is a former head of the Division of Nutrition and Chair of the Department of Environmental Health Sciences in the FSPH. 


  • PhD, Biochemistry and Nutrition, Cornell University, Ithaca, NY
  • MS, University of Arizona, Tucson, AZ
  • BS, Westminster College, New Wilmington, PA

Selected Publications

  • Eckhert, C. D. Boron Stimulates Embryonic Trout Growth. J. Nutrition 128:2488-2493, 1998.
  • Rowe, I. R., Bouzan, C., Nabili, S. and Eckhert, C.D. The response of trout and zebrafish embryos to low and high boron concentrations is U shaped. Biol. Trace Elem. Res. 66:262-270, 1998.
  • Rowe, R. I. Boron is required for zebrafish embryogenesis. J. Exp. Biol. 202:1649-1654, 1999.
  • Eckhert, C. D. and Rowe, R. I. Embryonic Dysplasia and Adult Retinal Dystrophy in Boron Deficient Zebrafish.  J. Trace Elements Exp. Med. 12: 1999.
  • Bennett, A., Rowe, R. I., Soch, N. and Eckhert, C. D. boron stimulates yeast (Saccharomyces cerevisiae) growth. J. Nutr.129:2236-2238, 1999.
  • Kim  D. H. S., Marbois B. N., Faull K. F., Eckhert C. D. Esterification of Borate with NAD+ and NADH as Studied by Electrospray Ionization Mass Spectrometry and 11B NMR Spectroscopy. J. Mass Spectrometry 38:632-640, 2003.
  • Cui Y. Winton M.I., Zhang, Z.F, Rainey C., Marshall J., deKernion J. B., Eckhert, C.D. Dietary Boron Intake and Reduced Risk of Prostate Cancer. Oncology Reports 11:887-892, 2004.
  • Barranco W.T. and Eckhert C.D. Boric acid inhibits human prostate cancer cell proliferation. Cancer Letters 216:21-29, 2004.
  • Kim D. H. S., Faull K. F., Norris A. J., Eckhert C. D. Borate-nucleotide complex formation depends on charge and phosphorylation state. J. Mass Spectrometry 39:743-751, 2004.
  • Barranco WT and Eckhert CD.  Cellular changes in boric acid-treated DU-145 prostate cancer cells.  Brit J. Cancer 94:884-890, 2006.
  • Kim DH, Que Hee S, Norris A, Faull KF and Eckhert CD.  Boric acid inhibits ADP-ribosyl cyclase non-competitively. J. Chromatography A.  1115:246-252, 2006. 
  • Barranco WT, Hudak PF and Eckhert CD. Evaluation of ecological and in vitro effects of boron on prostate cancer risk; Publisher Erratum Figure 1.  Cancer Causes Control.18:71-77, 2007.  Publisher Erratum Figure 1.  Cancer Causes Control.18:583-584, 2007.
  • Barranco WT, Kim DH, Stella SL, Eckhert CD. Boric acid inhibits the NAD+/CD38/cADPR Calcium Signaling Pathway.  Cell Biol Toxicol  DOI 10.1007/s10565-008-9085-7 (Published Online April 2008).
  • Henderson K, Stella SL Jr, Kobylewski S, Eckhert CD (2009) Receptor Activated Ca2+ Release Is Inhibited by Boric Acid in Prostate Cancer Cells. PLoS ONE 4(6): e6009. doi:10.1371/journal.pone.0006009
  • Yamada KE, Eckhert CD. Boric acid activation of eIF2 alpha and Nrf2 is PERK dependent: a mechanism that explains how boron prevents DNA damage and enhances antioxidant status. Biol Trace Ele Res. 188:2-10, 2019. DOI: 10.1007/s12011-018-1498-4. 
  • Eckhert CD. Trace Elements. In: Ross A.C., Caballero B, Cousins, R. J., Tucker K.L. ed. Modern Nutrition in Health and Disease. 11th ed. Baltimore: Williams & Wilkin, 2012.
  • Eckhert CD. Trace Elements. In: Modern Nutrition in Health and Disease. 12th ed.  Ross, A.C., Tucker K.L., Jensen G.L., Peterson K.E., Touger-Decker R., Duggan C.P. ed. Baltimore: Jones and Bartlett Learning, In Press 2023.