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PEMF Therapy - Some Things To Think About

This article is not medical or healthcare advice. Before starting any health or medical regimen you should the advice of your Primary Care Physician, or an M.D.

PEMF therapy has its own special legion of advocates. And its one of these 'gadgets' that is not in expensive enough to try on a whim. Its like an AMP Coil, you first find a friend with one - or a practitioner - and try it out. By far and away the biggest population of folks who are religious about its efficacy - are those recovery from Traumatic Brain Injury. Dr. Pawluk, appears to be the most well known, well established advocate for these devices, and he is easy to find.

How do these things work ? Well, if i had to summarize, its a combination of lowering oxidative stress, improving blood flow / circulation, and lowering platelet activation and what some call 'sticky red cells'. In the clinic i have an office at, i have used this on most in person clients, it is almost bullet proof to detect if the client has platelet activation issues along with a pulse oximeter. The response by folks if this issue is present is almost immediate and is often combined with oxygen from an oxygen concentrator, and often used prior to hyperbaric oxygen therapy.

Helps SOD2, Thirodoxin, Paraoxonases, and HSP 70 (Oxidative Stress)

"We found that PEMF treatment is able to quicken the in vitro repair of SkMC damage by increasing their proliferation and by increasing the production of proteins involved in the response to cellular damage and oxidative stress such as heat shock protein 70, superoxide dismutase 2, thioredoxin-1, and paraoxonases, We found that the expression of 10 proteins increased after two consecutive days of PEMF stimulation for 4 h, and most of them were involved in response processes to oxidative stress. Among these proteins, we found that heat shock protein 70 (HSP70), which can promote muscle recovery, inhibits apoptosis and decreases inflammation in skeletal muscle, together with thioredoxin, paraoxonase, and superoxide dismutase (SOD2), which can also promote skeletal muscle regeneration following injury. Altogether, these data support the possibility of using PEMF to increase SkMC regeneration and, for the first time, suggest a possible molecular mechanism, which consists of sustaining the expression of antioxidant enzymes to control the important inflammatory and oxidative process occurring following muscle damage.[1]

Helps Cerebral Ischema (Brain Injury - Impaired Blood Flow)

"Acute cerebral ischemia is characterized by several pathological processes evolving during time, which contribute to the final tissue damage. Secondary processes, such as prolonged inflammatory response, impaired mitochondrial function, and oxidative stress, are responsible for the progression of brain injury to the peri-infarct area, called “penumbra.” Adenosine has been shown to play a crucial role in regulating the inflammatory cascade following brain ischemia. Pulsed electromagnetic fields (PEMFs) act as modulators of adenosine receptors, increasing the functionality of the endogenous adenosine. In particular, PEMF exposure induces a significant upregulation of A2A and A3 adenosine receptors in different neuronal cell types. Several lines of evidence suggest that PEMF exposure might play a neuroprotective role after ischemic damage. "[2]

Helps LPS Induced Sepsis

"Despite advances in medicine, mortality due to sepsis has not decreased. Pulsed electromagnetic field (PEMF) therapy is emerging as an alternative treatment in many inflammation-related diseases. However, there are few studies on the application of PEMF therapy to sepsis. In the current study, we examined the effect of PEMF therapy on a mouse model of lipopolysaccharide (LPS)-induced septic shock. Mice injected with LPS and treated with PEMF showed higher survival rates compared with the LPS group. The increased survival was correlated with decreased levels of pro-inflammatory cytokine mRNA expression and lower serum nitric oxide levels and nitric oxide synthase 2 mRNA expression in the liver compared with the LPS group. In the PEMF + LPS group, there was less organ damage in the liver, lungs, spleen, and kidneys compared to the LPS group. To identify potential gene targets of PEMF treatment, microarray analysis was performed, and the results showed that 136 genes were up-regulated, and 267 genes were down-regulated in the PEMF + LPS group compared to the LPS group. These results suggest that PEMF treatment can dramatically decrease septic shock through the reduction of pro-inflammatory cytokine gene expression. In a clinical setting, PEMF may provide a beneficial effect for patients with bacteria-induced sepsis and reduce septic shock-induced mortality. "[3]

Nitric Oxide Production

"Our observations show that PEMF induce arteriolar dilation by an NO-dependent mechanism. Vasodilation leads to an increase in cerebral microvascular blood flow and, as a result, improved tissue oxygenation that persists for 3 hours......Thirty minutes of PEMF treatment induced cerebral arteriolar dilation leading to an increase in micro-vascular blood flow and tissue oxygenation that persisted for at least 3 hours. The effects of PEMF were mediated by NO, as we have shown in NOS inhibition experiments.[4]


  1. Pulsed Electromagnetic Fields Induce Skeletal Muscle Cell Repair by Sustaining the Expression of Proteins Involved in the Response to Cellular Damage and Oxidative Stress

  2. Review ArticlePulsed Electromagnetic Fields: A Novel Attractive Therapeutic Opportunity for Neuroprotection After Acute Cerebral Ischemia. Neuromodulation: Technology at the Neural Interface. Volume 25, Issue 8, December 2022, Pages 1240-1247.

  3. Pulsed Electromagnetic Field (PEMF) Treatment Reduces Lipopolysaccharide-Induced Septic Shock in Mice. by Chang-Gun Lee, Chanoh Park. Int. J. Mol. Sci. 2022, 23(10), 5661; Submission received: 24 April 2022 / Revised: 14 May 2022 / Accepted: 17 May 2022 / Published: 18 May 2022

  4. Increases in microvascular perfusion and tissue oxygenation via pulsed electromagnetic fields in the healthy rat brain. Denis E. Bragin, PhD,1,2 Gloria L. Statom, J Neurosurg. Author manuscript; available in PMC 2019 Jan 5. J Neurosurg. 2015 May; 122(5): 1239–1247.

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