Objective

• Apply non-contact biofield therapy in varying dosages at the world’s largest cancer center to the world’s most deadly cancer in a series of controlled preclinical studies including repeated invitro experiments in human and mouse cancer cell lines, patient derived organoids, and mouse studies, using a pre-registered protocol, full blinding, and multiple controls
• As a continuation of the prior research study which confirmed biofield therapy’s antitumor and antimetastatic efficacy and mechanism in cancer invitro, the second phase is to further investigate efficacy and mechanism invivo, as well as to further investigate the nature of the biofield healing signal through blocking, distance, EEG, and quantum entanglement studies

Hypothesis

• Biofield therapy reduces xenograft tumorigenesis (tumor formation) and metastases (tumor spread) across a number of cancer types invivo to a greater extent than conventional treatment.  This will be detectable not only through tumor remission/reduction but also via various biological markers
• Biofield therapy functions by modulating oncogenic pathways, their downstream targets, and the tumor microenvironment
• Biofield therapy is mediated by electromagnetic frequencies, gauged by whether EMF shielding attenuates the biofield healing effect
• A second biofield therapist will have similar efficacy outcomes in select invitro and invivo animal models, demonstrating a generalizable effect across biofield therapists

Outcomes

• In replicating the prior biofield therapy experiments, confirmed efficacy of biofield therapy with antiproliferative effects and antimetastatic effects across three different biofield therapists, 6+ types of pancreatic cells, and in 2 types of mice:
  • Consistently reduced the growth rate in cancer cells and patient-derived tumor organoids statistically significantly relative to controls
  • Inhibited spread (metastasis), with migration and invasion through tissue barriers in pancreatic cells statistically reduced relative to controls, by 34-55% in cells, stopping cell cycle progression early and dramatically decreasing spread to surrounding cells better than today’s standard of care drug, gemcitabine
  • In three different mouse experiments, biofield therapy substantially reduced metastasis from the pancreas to the liver, including a ~70-75% reduction in the number of metastatic liver nodules in some studies and market reductions in overall liver tumor burden in others, which are antimetastatic effects comparable to chemotherapy
  • Growth suppressing effects were seen across cancer cell types but not in normal pancreatic cells, suggesting that biofield therapy preferentially targets cancer tumor cells
  • The measurable biological changes from biofield therapy are independent of placebo effect, as they were conducted in cell cultures and animals
• Determined biochemically mediated mechanisms of action of biofield therapy on pancreatic cancer invitro and invivo observing:
  • Visibly damaged mitochondrial structures (the cell’s energy producing structures), significantly swollen and disrupted, indicating cellular stress or dysfunction
  • Cancer cells stuck in neutral, with an increased proportion of cancer cells in the resting (G0/G1) phase of the cell cycle, limiting their ability to divide and proliferate
  • Cell electrical properties altered from an electrically active (“depolarized”) state to less active, more stable (“depolarized”) state. Abnormal electrical activity was reduced by 30-50% in multiple cell lines, a shift associated with slower growth and reduced ability of cancer cells to migrate and spread
  • Critical growth protein FOXM1, a key driver of cancer growth and metastasis, was suppressed Modulated expression of FOXM1. When FOXM1 was genetically removed, many of biofield therapy’s effects were diminished, which suggests that the biofield therapy-induced anti-proliferative, anti-metastatic effect may be at least in part mediated by its ability to downregulate the FOXM1 protein
  • Altered immune cell profile in mice, turning on the immune function to kill cancer cells
• Replicated the results with a second biofield therapist invitro and in invivo animal models with consistent outcomes
• Evaluated whether biofield therapy is mediated by electromagnetic frequencies (EMFs) with EMF shielding and distance experimentation with no blocking or attenuation of effect.
• Observed correlated healer EEG and pancreatic cell-level signaling, in a way that suggests bidirectional informational exchange/influence, perhaps a form of entanglement which requires further research in the subsequent stage
• Biofield therapy appears to influence pancreatic cancer at a fundamental level, including cellular energy systems, electrical signaling, and gene regulation pathways (notably FOXM1), leading to reduced proliferation and invasiveness. These effects occur without direct physical interaction with the cells or animals, supporting the hypothesis that biofield-based interactions may influence biological systems, a potentially promising complementary approach worthy of further preclinical and clinical investigation

Publication in Cancer Medicine:

The Preclinical Effects and Mechanisms of Biofield Therapy on Pancreatic Cancer Cell Growth and Metastasis

Publication in Biophysica:

Search for Entanglement between Spatially Separated Living Systems: Experiment Design, Results, and Lessons Learned

Publication in Nature’s Scientific Reports

Examining the effects of biofield therapy through simultaneous assessment of electrophysiological and cellular outcomes

Further publications are in process