Low-energy Pulsed Electromagnetic Fields Research Articles

Brief, weekly magnetic muscle therapy improves mobility and lean body mass in older adults: a Southeast Asia community case study

Brief (10 min) weekly exposure to low energy pulsed electromagnetic fields (PEMFs) has been shown to improve human muscle mitochondrial bioenergetics and attenuate systemic lipotoxicity following anterior cruciate ligament surgical reconstruction. Here we present data generated from 101 participants, 62% female, aged 38-91 years, recruited from the QuantumTx Demo Centre in Singapore, wherein 87% of participants (n = 88) presented with pre-existing mobility dysfunction and 13% (n = 13) were healthy volunteers. Participants were recruited if: (i) not pregnant; (ii) above 35 years of age and; (iii) without surgical implants. All participants completed mobility testing, pre- and post- PEMF intervention for 12 weeks, whereas bioelectrical impedance analysis was conducted in a subgroup of 42 and 33 participants at weeks 4 and 8, respectively. Weekly PEMF exposure was associated with significant improvements in mobility (Timed Up and Go, 5 times Sit-to-Stand, and 4m Normal Gait Speed) and body composition (increased skeletal muscle mass and reduced total and visceral fat mass), particularly in the older participants. Perception of pain was also significantly reduced. PEMF therapy may provide a manner to counteract age-associated mobility and metabolic disruptions and merits future investigation in randomized controlled trials to elucidate its clinical benefits in the frail and older adult populations.

Low-energy Pulsed Electromagnetic Field Therapy Reduces Pain in Fibromyalgia: A Randomized Single-blind Controlled Pilot Study.

Fibromyalgia symptoms have a significant impact on the quality of life and respond poorly to medications. It has been hypothesized that the use of low-energy pulsed electromagnetic field (PEMF) induces neuroprotective effects that may interfere with pain perception. We explored the efficacy of PEMF in patients affected by fibromyalgia. Twenty-one females (median age 59 years, interquartile range [IQR] 16.5) affected by fibromyalgia were randomized to receive pulsed electromagnetic field-triple energy pain treatment (PEMF-TEPT) or placebo at T0 and at 4 weeks and 8 weeks. Fibromyalgia impact questionnaire (FIQ), widespread pain index (WPI), visual analog score (VAS) pain, symptom severity (SS) scale, and short form 36 (SF-36) health survey questionnaire have been evaluated. Patients in the PEMF-TEPT group had a significantly higher reduction of WPI compared to placebo (mean difference -12.90 ± standard deviation [SD] 5.32 vs. -1.91 ± 4.55, difference in difference [DD] of -10.99; P < 0.001), of SS score (-4.10 ± 4.85 vs. -2.00 ± 2.32; DD = -2.1; P < 0.05), of VAS pain (-48 ± 30.75 vs. -16.82 ± 23.69; DD = -31.18; P < 0.01). They also reported a higher improvement of FIQ and SF-36, albeit not reaching statistical significance. In our pilot controlled study, PEMF-TEPT appeared to be safe and improved fibromyalgia symptoms.

The influence of pulsed electromagnetic field therapy (PEMFT) on cutaneous blood flow in healthy volunteers1.

The biophysical interaction induced by low energy pulsed electromagnetic field therapy (PEMFT) on the capillary microcirculation is not well understood. Several studies indicate a significant effect of PEMFT in patients with chronic medical conditions. The aim of this study was to evaluate the influence of PEMFT on skin microcirculation in healthy volunteers. 15 healthy participants were included. Nine PEMF treatments were applied over three weeks in an 48-hour interval. The PEMFT system (BEMER) was placed beneath one of the participants' leg with the contralateral side serving as a control. A forty-minute application period was preceded by a 10-minute resting phase. Measuring was done using two Laser Doppler probes (LEA) placed on each anterior lateral thigh. All outcome parameters including flow, mixed venous oxygen saturation and relative venous hemoglobin showed a significant increase during the experiment when compared to the baseline values of the resting phase in both groups (p < 0.01). Comparing both groups, the measurement values during the experiment did not differ (p > 0.05) except for higher flow values in the control group (P = 0.03). Over time, baseline values of both groups showed no significant difference (p > 0.05). We found a significant increase of all measurement parameters during the study compared to the baseline values with no difference between the PEMF and control group.

Signaling pathways involved in anti-inflammatory effects of Pulsed Electromagnetic Field in microglial cells

Literature studies suggest important protective effects of low-frequency, low-energy pulsed electromagnetic fields (PEMFs) on inflammatory pathways affecting joint and cerebral diseases. However, it is not clear on which bases they affect neuroprotection and the mechanism responsible is yet unknown. Therefore the aim of this study was to identify the molecular targets of PEMFs anti-neuroinflammatory action. The effects of PEMF exposure in cytokine production by lipopolysaccharide (LPS)-activated N9 microglial cells as well as the pathways involved, including adenylyl cyclase (AC), phospholipase C (PLC), protein kinase C epsilon (PKC-ε) and delta (PKC-δ), p38, ERK1/2, JNK1/2 mitogen activated protein kinases (MAPK), Akt and caspase 1, were investigated. In addition, the ability of PEMFs to modulate ROS generation, cell invasion and phagocytosis, was addressed. PEMFs reduced the LPS-increased production of TNF-α and IL-1β in N9 cells, through a pathway involving JNK1/2. Furthermore, they decreased the LPS-induced release of IL-6, by a mechanism not dependent on AC, PLC, PKC-ε, PKC-δ, p38, ERK1/2, JNK1/2, Akt and caspase 1. Importantly, a significant effect of PEMFs in the reduction of crucial cell functions specific of microglia like ROS generation, cell invasion and phagocytosis was found. PEMFs inhibit neuroinflammation in N9 cells through a mechanism involving, at least in part, the activation of JNK MAPK signalling pathway and may be relevant to treat a variety of diseases characterized by neuroinflammation.

Pulsed electromagnetic field and relief of hypoxia-induced neuronal cell death: The signaling pathway.

Low-energy low-frequency pulsed electromagnetic fields (PEMFs) exert several protective effects, such as the regulation of kinases, transcription factors as well as cell viability in both central and peripheral biological systems. However, it is not clear on which bases they affect neuroprotection and the mechanism responsible is yet unknown. In this study, we have characterized in nerve growth factor-differentiated pheochromocytoma PC12 cells injured with hypoxia: (i) the effects of PEMF exposure on cell vitality; (ii) the protective pathways activated by PEMFs to relief neuronal cell death, including adenylyl cyclase, phospholipase C, protein kinase C epsilon and delta, p38, ERK1/2, JNK1/2 mitogen-activated protein kinases, Akt and caspase-3; (iii) the regulation by PEMFs of prosurvival heat-shock proteins of 70 (HSP70), cAMP response element-binding protein (CREB), brain-derived neurotrophic factor (BDNF), and Bcl-2 family proteins. The results obtained in this study show a protective effect of PEMFs that are able to reduce neuronal cell death induced by hypoxia by modulating p38, HSP70, CREB, BDNF, and Bcl-2 family proteins. Specifically, we found a rapid activation (30 min) of p38 kinase cascade, which in turns enrolles HSP70 survival chaperone molecule, resulting in a significant CREB phosphorylation increase (24 hr). In this cascade, later (48 hr), BDNF and the antiapoptotic pathway regulated by the Bcl-2 family of proteins are recruited by PEMFs to enhance neuronal survival. This study paves the way to elucidate the mechanisms triggered by PEMFs to act as a new neuroprotective approach to treat cerebral ischemia by reducing neuronal cell death.

Pulsed electromagnetic field therapy in the treatment of pain and other symptoms in fibromyalgia: A randomized controlled study.

Low-energy pulsed electromagnetic field (PEMF) therapy has been suggested as a promising therapy to increase microcirculation, which is of great concern in patients with fibromyalgia. This study evaluated the effectiveness of PEMF therapy on the treatment of fibromyalgia. A group of 108 women with fibromyalgia were allocated to a 12-week treatment period with an active Bio-Electro-Magnetic-Energy-Regulation (BEMER) device and a similar treatment period with an inactive device. Each patient received active and sham treatments in a random order. Pain and stiffness were assessed on a visual analog scale (VAS, scale 0-100 mm), and functional status was assessed by the Fibromyalgia Impact Questionnaire (FIQ). Mean VAS pain scores before the active and sham treatment periods were 66 (SD 22) and 63 (SD 22), respectively. After treatment periods, mean VAS pain scores had decreased significantly in active treatment, -12, 95% CI [-18, -6], and in sham treatment, -11, 95% CI [-17, -5]. Similarly, the decrease in stiffness and FIQ index after both treatments was statistically significant. However, per-protocol analysis showed no differences between active and sham treatments at any of the outcomes. This study demonstrated that low-energy PEMF therapy was not efficient in reducing pain and stiffness or in improving functioning in women with fibromyalgia. Bioelectromagnetics. 39:405-413, 2018. © 2018 Wiley Periodicals, Inc.

Adenosine Receptors as a Biological Pathway for the Anti-Inflammatory and Beneficial Effects of Low Frequency Low Energy Pulsed Electromagnetic Fields.

Several studies explored the biological effects of low frequency low energy pulsed electromagnetic fields (PEMFs) on human body reporting different functional changes. Much research activity has focused on the mechanisms of interaction between PEMFs and membrane receptors such as the involvement of adenosine receptors (ARs). In particular, PEMF exposure mediates a significant upregulation of A2A and A3ARs expressed in various cells or tissues involving a reduction in most of the proinflammatory cytokines. Of particular interest is the observation that PEMFs, acting as modulators of adenosine, are able to increase the functionality of the endogenous agonist. By reviewing the scientific literature on joint cells, a double role for PEMFs could be hypothesized in vitro by stimulating cell proliferation, colonization of the scaffold, and production of tissue matrix. Another effect could be obtained in vivo after surgical implantation of the construct by favoring the anabolic activities of the implanted cells and surrounding tissues and protecting the construct from the catabolic effects of the inflammatory status. Moreover, a protective involvement of PEMFs on hypoxia damage in neuron-like cells and an anti-inflammatory effect in microglial cells have suggested the hypothesis of a positive impact of this noninvasive biophysical stimulus.

Pulsed Electromagnetic Field Exposure Reduces Hypoxia and Inflammation Damage in Neuron-Like and Microglial Cells.

In the present study, the effect of low-frequency, low-energy pulsed electromagnetic fields (PEMFs) has been investigated by using different cell lines derived from neuron-like cells and microglial cells. In particular, the primary aim was to evaluate the effect of PEMF exposure in inflammation- and hypoxia-induced injury in two different neuronal cell models, the human neuroblastoma-derived SH-SY5Y cells and rat pheochromocytoma PC12 cells and in N9 microglial cells. In neuron-like cells, live/dead and apoptosis assays were performed in hypoxia conditions from 2 to 48 h. Interestingly, PEMF exposure counteracted hypoxia damage significantly reducing cell death and apoptosis. In the same cell lines, PEMFs inhibited the activation of the hypoxia-inducible factor 1α (HIF-1α), the master transcriptional regulator of cellular response to hypoxia. The effect of PEMF exposure on reactive oxygen species (ROS) production in both neuron-like and microglial cells was investigated considering their key role in ischemic injury. PEMFs significantly decreased hypoxia-induced ROS generation in PC12, SH-SY5Y, and N9 cells after 24 or 48 h of incubation. Moreover, PEMFs were able to reduce some of the most well-known pro-inflammatory cytokines such as tumor necrosis factor-α (TNF-α), interleukin (IL)-1β, IL-6, and IL-8 release in N9 microglial cells stimulated with different concentrations of LPS for 24 or 48 h of incubation time. These results show a protective effect of PEMFs on hypoxia damage in neuron-like cells and an anti-inflammatory effect in microglial cells suggesting that PEMFs could represent a potential therapeutic approach in cerebral ischemic conditions. J. Cell. Physiol. 232: 1200-1208, 2017. © 2016 Wiley Periodicals, Inc.

Chondroprotective effects of low-frequency lowenergy pulsed electromagnetic fields on human cartilage explants

Objective To investigate the effects of low-frequency low-energy pulsed electromagnetic fields (PEMFs) on proteoglycans (PG) metabolism [1-2] of human articular cartilage explants derived from patients with different osteoarthritis (OA) grades in the presence and in the absence of anabolic and catabolic stimuli for cartilage. Design Human knee cartilage explants derived from lateral and medial femoral condyles of OA patients were exposed to PEMF (1.5 mT; 75 Hz) for 1 and 7 days with and without insulin-like growth factor-I (IGF-I) (50 ng/ml) and interleukin-1β (IL-1β) (0.01-50ng/ml). Histological analysis was used to classify cartilage according to the score developed by the International Cartilage Repair Society (ICRS). PG synthesis was determined by 35S-sulfate incorporation. PG release into culture media was determined by the dimethylmethylene blue assay. Results By histological evaluation, cartilage explants derived from lateral and medial condyles were classified as OA ICRS grade I and III, respectively. After 7 days treatment, in OA grade I cartilage explants, PEMF and IGF-I alone significantly increased 35S-sulfate incorporation respect to control and counteracted the effect induced by IL-1β (0.01 ng/ml) of 26% and 24% respectively. The combination of PEMF and IGF-I resulted additive in all conditions. Similar results were obtained in OA grade III cartilage, although basal 35S-sulfate incorporation was lower than in OA grade I. No effect was observed on medium PG release. Conclusions PEMF exerts chondroprotective effects on human articular cartilage. The biological responsiveness of chondrocyte to PEMF was similar in different OA grades cartilage, suggesting that human chondrocytes maintain susceptibility to PEMF during OA progression.

Characterization of adenosine receptors in bovine chondrocytes and fibroblast-like synoviocytes exposed to low frequency low energy pulsed electromagnetic fields

The present study describes the presence and binding parameters of the A1, A2A, A2B and A3 adenosine receptors in bovine chondrocytes and fibroblast-like synoviocytes. The effect of low frequency low energy pulsed electromagnetic fields (PEMFs) on the adenosine receptor affinity and density was studied. Saturation, competition binding experiments and Western blotting assays in the absence and in the presence of PEMFs on the adenosine receptors in bovine chondrocytes or fibroblast-like synoviocytes were performed. Thermodynamic analysis of the A2A or A3 binding was studied to investigate the forces driving drug-receptor coupling. In the adenylyl cyclase and proliferation assays the potency of typical high-affinity A2A or A3 agonists in the absence and in the presence of PEMFs was evaluated. Bovine chondrocytes and fibroblast-like synoviocytes expressed all adenosine receptors. PEMFs evoked an up-regulation of A2A and A3 receptors and thermodynamic parameters indicate that adenosine binding is enthalpy and entropy driven. In PEMF-treated cells the potency of typical A2A or A3 agonists on cyclic AMP assays was significantly increased when compared with the untreated cells. PEMFs potentiated the effect of A2A or A3 agonists on cell proliferation in both cell types. PEMFs mediate an up-regulation of A2A and A3 receptors related to an increase of their functional activities in bovine chondrocytes and fibroblast-like synoviocytes. No differences are present in adenosine affinity and in the drug-receptor interactions. Our data could be used as a trigger to future studies addressed to PEMFs and adenosine therapeutic intervention in inflammatory joint diseases.

Proteoglycan synthesis in bovine articular cartilage explants exposed to different low-frequency low-energy pulsed electromagnetic fields

To investigate the role of pulsed electromagnetic field (PEMF) exposure parameters (exposure length, magnetic field peak amplitude, pulse frequency) in the regulation of proteoglycan (PG) synthesis of bovine articular cartilage explants. Bovine articular cartilage explants were exposed to a PEMF (75 Hz; 2 mT) for different time periods: 1, 4, 9, 24 h. Then, cartilage explants were exposed for 24 h to PEMFs of different magnetic field peak amplitudes (0.5, 1, 1.5, 2 mT) and different frequencies (2, 37, 75, 110 Hz). PG synthesis of control and exposed explants was determined by Na2-35SO4 incorporation. PEMF exposure significantly increased PG synthesis ranging from 12% at 4 h to 17% at 24 h of exposure. At all the magnetic field peak amplitude values, a significant PG synthesis increase was measured in PEMF-exposed explants compared to controls, with maximal effect at 1.5 mT. No effect of pulse frequency was observed on PG synthesis stimulation. The results of this study show the range of exposure length, PEMF amplitude, pulse frequency which can stimulate cartilage PG synthesis, and suggest optimal exposure parameters which may be useful for cartilage repair in in vivo experiments and clinical application.

Bone mass is preserved in a critical-sized osteotomy by low energy pulsed electromagnetic fields as quantitated by in vivo micro-computed tomography

The effectiveness of non-invasive pulsed electromagnetic fields (PEMF) on stimulating bone formation in vivo to augment fracture healing is still controversial, largely because of technical ambiguities in data interpretation within several previous studies. To address this uncertainty, we implemented a rigorously controlled, blinded protocol using a bilateral, mid-diaphyseal fibular osteotomy model in aged rats that achieved a non-union status within 3–4 weeks post-surgery. Bilateral osteotomies allowed delivery of a PEMF treatment protocol on one hind limb, with the contralateral limb representing a within-animal sham-treatment. Bone volumes in both PEMF-treated and sham-treated fibulae were assessed simultaneously in vivo using highly sensitive, high-resolution micro-computed tomography (μCT) over the course of treatment. We found a significant reduction in the amount of time-dependent bone volume loss in PEMF-treated, distal fibular segments as compared to their contralateral sham-treated bones. Osteotomy gap size was significantly smaller in hind limbs exposed to PEMF over sham-treatment. Therefore, our data demonstrate measurable biological consequences of PEMF exposure on in vivo bone tissue.

IN VITROEFFECTS OF PEMFs ON BONE CELL CULTURES OF NORMAL AND OSTEOPENIC RAT

The aim of this study was to examine the effects of low-frequency, low-energy pulsed electromagnetic fields (PEMFs) on cell proliferation and differentiation in rat osteoblast primary cultures. Cells were obtained from normal and osteopenic rat bone and were named NB and OB, respectively. The osteoblastic phenotype was assessed by stimulation with 1,25(OH2) vitamin D3. NB and OB cells were seeded in multiwell plates and exposed to PEMFs for two different periods. Control cultures of both groups were incubated under the same conditions, with the pulse generator off. Assessment of PEMF effects was performed for the following parameters for each culture: alkaline phosphatase (ALP) activity, osteocalcin level, and MTT test. Results showed that OB and NB cell proliferation was significantly improved (p < 0.03, p = 0.04 respectively) after 48 h of PEMF exposure. Osteocalcin production of OB after 5 days of PEMF exposure was significantly higher than normal (p = 0.007) and osteopenic (p = 0.033) bone-derived controls. These results show that PEMFs act on osteopenic bone-derived osteoblasts, stimulating proliferation of cells and then, after a longer exposure, activating them.

Effects of Low-Frequency Pulsed Electromagnetic Fields on Human Osteoblast-Like CellsIn Wtro

We have studied the effects of low-frequency, low-energy pulsed electromagnetic fields (PEMFs) on human osteoblast-like cells in vitroin order to investigate the biochemical mechanism(s) by which electrical stimulation can effect changes in skeletal metabolism. Bony nature of the cells was assayed by immunolabeling with antiosteonectin antibody. Multidish plates were placed between a pair of Helmoltz coils powered by a pulse generator (1.3 ms, 75 Hz) in a tissue culture incubator for 24 h. 3H-thymidine was added to the culture medium to evaluate cell proliferation. The acid-precipitable 3H-thymidine incorporation significantly increases in PEMF-exposed cells as compared to the control. PEMF exposure induces a two- to fivefold increase of DNA synthesis. Osteoblasts cultured for 24 h in a serum-free medium show a very low proliferation rate, and the exposure to PEMF does not stimulate DNA synthesis.

The Effects of Pulsating Electromagnetic Fields on Differentiation and Growth in Cloudman S91 Murine Melanoma Cells in vitro

Specific low-energy pulsed electromagnetic fields (PEMF) induced, in certain circumstances, changes in the activity of tyrosine hydroxylase (a marker for differentiation), the level of melanin (correlating with the tyrosine hydroxylase activity), the level of cAMP, and mitosis, in Cloudman S91 clone M3 murine melanoma cells. The observed changes were similar to those induced by alpha melanocyte stimulating hormone (MSH). A specific PEMF caused an additive increase in tyrosine hydroxylase, and an additive decrease in mitosis with MSH and activators of adenylate cyclase. Continuously applied PEMF throughout the culture period inhibited tyrosine hydroxylase but not cell division. In cultures passaged for more than about 39 times, a loss of tyrosine hydroxylase response but not mitotic response to MSH occurred. This loss of tyrosinase response to MSH correlated with a loss of response to PEMF but both MSH and PEMF inhibited mitosis to the same extent as in earlier passage cells. The inhibition of mitosis by P...