The use of electromagnetic fields to manipulate cellular biochemistry in favorable ways is a field very much in its infancy in comparison to the well established use of small molecule drugs. At the high level, it is quite similar to exploration with small molecules, in that there is a great deal of freedom to experiment with parameters: intensity, frequency, duration, dosing, a focus on primarily electrical versus primarily magnetic fields, equipment differences, and so forth. Within that vast parameter space, only some combinations will be useful. In general this part of the field is characterized by results that fail to replicate and incomplete information on all of the parameters needed to recreate the exact protocol used. Nonetheless, there are some areas of promise where multiple research groups have achieved positive results, and even brought the work into human trials. The use of electric fields to stimulate more rapid regeneration from injury is one example.
Today’s open access paper reports on the use of magnetic fields to stimulate beneficial changes in mitochondrial function that are similar to those that occur following exercise. The authors term it magnetic mitohormesis, and one might take a look at an earlier review paper that discusses the mechanisms thought to be involved. The hundreds of bacteria-like mitochondria present in every cell are vital to cell function, primarily by producing adenosine triphosphate (ATP), a chemical energy store molecule. A vast body of evidence indicates that mitochondrial function declines with age, while the various strategies available to modestly improve mitochondrial function, including exercise, are beneficial to health and slow aging to some degree, at least in animal studies, in part because they improve mitochondrial function.
We, and others, have shown that brief exposures to pulsed electromagnetic fields (PEMF) stimulate mitochondrial respiration via a calcium-mitochondrial axis upstream to PGC-1α transcriptional regulation and recreate biological and metabolic adaptations similar to endurance exercise but without physical stress or strain.
In pre-clinical murine studies, PEMF exposure was shown to activate muscle mitochondrial respiration to induce exercise-related muscle adaptation and mitochondrial biogenesis. These responses resulted in the manifestation of typically exercise-associated positive metabolic adaptations, including improved insulin sensitivity, reduced resting insulin levels, enhanced fatty acid oxidation, and enhanced oxidative muscle expression downstream of the well-established pro-metabolic health pathways largely governed by PGC-1α co-transcriptional regulation.
Related benefits have also been observed in several published human studies employing this same PEMF exposure paradigm. In elderly patients, brief 10-min weekly PEMF treatment for 12 weeks increased skeletal mass and reduced total and visceral adiposity. More recently, it was found that PEMF treatment improved knee muscle strength and reduced pain in elderly patients with end-stage osteoarthritis of the knees. In another example, weekly treatment with PEMF for 16 weeks improved markers of muscle mitochondrial functioning and lowered systemic lipotoxicity in patients who underwent anterior cruciate ligament reconstruction compared to placebo.
Collectively, these data support the ability of PEMF treatment to replicate the metabolic benefits of endurance exercise. However, it is unknown whether low-dose PEMF treatment, which we will refer to as magnetic mitohormesis (MM), improves diabetes control. In this open-labeled exploratory study, we investigated the impact of MM on metabolic control in patients with suboptimally-controlled type 2 diabetes mellitus (T2DM). In addition, because PEMF treatment has been shown to reduce visceral fat, we examined whether patients with central obesity (defined as waist-to-hip ratio, WHR of ≥1.0) exhibit a greater propensity to benefit more from this treatment.
The 40 participants had a mean age of 59.4 years and HbA1c of 8.1%. MM treatment was well tolerated with no adverse events, and 77.5% of patients completed all 12 sessions. There were no significant changes in HbA1c, fasting glucose, or HOMA-IR for the overall cohort. However, in patients with central obesity, 88.9% showed a reduction in HbA1c post-treatment compared to 32.3% without central obesity, and mean HbA1c decreased from 7.5% to 7.1%. Our findings suggest that MM is safe and well-tolerated in T2DM patients and may confer a preferential benefit for individuals with greater central obesity.
