Dr. Oz recently featured PEMF (pulsed electromagnetic field) therapy and is quoted as saying that "This will change medicine". Although you may have never heard of PEMF there are thousands of research papers that prove it's effectiveness in helping treat chronic disease and injury, in fact the FDA has approved PEMF therapy for use in healing bones. But don't just take my word for it, go to the government website, www.pubmed.gov and type in "PEMF"in the search bar at the top of the screen. The result will impress you. I am so proud and excite to announce that we are bringing this treatment to Southwest Florida. If you or anyone you know is suffering with pain or has an injury that just won't heal, please pass this information along to them so they can try this amazing procedure.
Every cell in the body is designed to run at -20 to -25 millivolts. To heal, we must make new cells. To make a new cell requires -50 millivolts. Chronic disease occurs when voltage drops below -20 and/or you cannot achieve -50 millivolts to make new cells. Thus chronic disease is always defined by having low voltage. PEMF help to charge up your cells, giving them more potential for healing. This actually helps your body heal the damage without dangerous drugs or invasive surgeries. This is a safe and easy treatment to receive. Most patients experience a change after the very first session.
PEMF USED IN BRAIN DISORDERS
PEMF CREATES ANGIOGENESIS
As tissue responds to injury, PEMF can rapidly modulate the relaxation of the smooth muscles controlling blood and lymph vessel tone through the CaM/NO/cGMP cascade (McKay et al., 2007). PEMF also enhances growth factor release through the same cascade in endothelial cells to modulate angiogenesis. PEMF modulation of eNOS activity may, therefore, be a useful strategy to augment angiogenesis for tissue repair and possibly other conditions that require vascular plasticity, such as ischemia (Cooke, 2003).
Quantification of angiogenic proteins demonstrated a sevenfold increase in FGF-2, suggesting that PEMF modulates angiogenesis by increasing FGF-2 production. This same study also reported PEMF increased vascular ingrowth more than twofold when applied to an implanted Matrigel plug in mice, with a concomitant increase in FGF-2, similar to that observed in vitro. PEMF significantly increased neovascularization and wound repair in normal mice, and particularly in diabetic mice, through an endogenous increase in FGF-2, which could be eliminated by using a FGF-2 inhibitor (Callaghan et al., 2008). Similarly, a PEMF signal of the type used clinically for wound repair was reported to significantly accelerate vascular sprouting from an arterial loop transferred from the hind limb to the groin in a rat model (Roland et al., 2000). This study suggests a significant clinical application for PEMF signals in reconstructive surgery.
Another study (Delle Monache et al., 2008) reported that PEMF increased the degree of endothelial cell proliferation and tubule formation and accelerated the process of wound repair, suggesting a mechanism based upon a PEMF effect on VEGF receptors. In the clinical setting, PEMF has been reported to enhance fresh and chronic wound repair (Kloth et al., 1999; Kloth and Pilla, 2010; Strauch et al., 2007; Guo et al., 2012). A recent study evaluated the effect of PEMF on cardiac angiogenesis in a reproducible thermal myocardial injury model. The injury was created in the region of the distal aspect of the left anterior descending artery at the base of the heart in a blinded rat model (Patel et al., 2006; Strauch et al., 2006, 2009; Pilla, 2013). PEMF exposure was 30 min twice daily for 3, 7, 14, or 21 days. Sham animals were identically exposed, but received no PEMF signal. A separate group of animals treated for 7 days received L-nitroso-arginine methyl ester (L-NAME), a general NOS inhibitor, in their drinking water. Upon sacrifice, myocardial tissue specimens were stained with CD-31, and the number of new blood vessels was counted on histological sections at the interface between normal and necrotic muscle at each time point by three independent blinded histologists. The results showed mean new vessel count was not signi cantly increased by PEMF at day 3, but was signi cantly increased at day 7 (+50%, P = 0.006), day 14 (+67%, P = 0.004), and day 21 (+99%, P < 0.001). The results for day 7 indicate L-NAME completely blocked the PEMF effect on angiogenesis, suggesting the transduction pathway for the PRF effect on angiogenesis in this study involved CaM- dependent NO signaling.