Cancer cell proliferation is inhibited by specific modulation frequencies.

BACKGROUND: There is clinical evidence that very low and safe levels of amplitude-modulated electromagnetic fields administered via an intrabuccal spoon-shaped probe may elicit therapeutic responses in patients with cancer. However, there is no known mechanism explaining the anti-proliferative effect of very low intensity electromagnetic fields. METHODS: To understand the mechanism of this novel approach, hepatocellular carcinoma (HCC) cells were exposed to 27.12 MHz radiofrequency electromagnetic fields using in vitro exposure systems designed to replicate in vivo conditions. Cancer cells were exposed to tumour-specific modulation frequencies, previously identified by biofeedback methods in patients with a diagnosis of cancer. Control modulation frequencies consisted of randomly chosen modulation frequencies within the same 100 Hz-21 kHz range as cancer-specific frequencies. RESULTS: The growth of HCC and breast cancer cells was significantly decreased by HCC-specific and breast cancer-specific modulation frequencies, respectively. However, the same frequencies did not affect proliferation of nonmalignant hepatocytes or breast epithelial cells. Inhibition of HCC cell proliferation was associated with downregulation of XCL2 and PLP2. Furthermore, HCC-specific modulation frequencies disrupted the mitotic spindle. CONCLUSION: These findings uncover a novel mechanism controlling the growth of cancer cells at specific modulation frequencies without affecting normal tissues, which may have broad implications in oncology.

Treatment of advanced hepatocellular carcinoma with very low levels of amplitude-modulated electromagnetic fields.

BACKGROUND: Therapeutic options for patients with advanced hepatocellular carcinoma (HCC) are limited. There is emerging evidence that the growth of cancer cells may be altered by very low levels of electromagnetic fields modulated at specific frequencies. METHODS: A single-group, open-label, phase I/II study was performed to assess the safety and effectiveness of the intrabuccal administration of very low levels of electromagnetic fields amplitude modulated at HCC-specific frequencies in 41 patients with advanced HCC and limited therapeutic options. Three-daily 60-min outpatient treatments were administered until disease progression or death. Imaging studies were performed every 8 weeks. The primary efficacy end point was progression-free survival 6 months. Secondary efficacy end points were progression-free survival and overall survival. RESULTS: Treatment was well tolerated and there were no NCI grade 2, 3 or 4 toxicities. In all, 14 patients (34.1%) had stable disease for more than 6 months. Median progression-free survival was 4.4 months (95% CI 2.1-5.3) and median overall survival was 6.7 months (95% CI 3.0-10.2). There were three partial and one near complete responses. CONCLUSION: Treatment with intrabuccally administered amplitude-modulated electromagnetic fields is safe, well tolerated, and shows evidence of antitumour effects in patients with advanced HCC.

Effects of low energy emission therapy in chronic psychophysiological insomnia.

The treatment of chronic psychophysiological insomnia presents a challenge that has not been met using currently available pharmacotherapy. Low energy emission therapy (LEET) has been developed as a potential alternative therapy for this disorder. LEET consists of amplitude-modulated electromagnetic fields delivered intrabuccally by means of an electrically conducting mouthpiece in direct contact with the oral mucosa. The effect of LEET on chronic psychophysiological insomnia was assessed with polysomnography (PSG) and sleep rating forms on a total of 106 patients at two different centers. Active or inactive LEET was administered for 20 minutes in late afternoon three times a week for a total of 12 treatments. Primary efficacy endpoints evaluating the results were changes from baseline in PSG-assessed total sleep time (TST) and sleep latency (SL). Secondary endpoints were changes in sleep efficiency (SE), sleep stages, and reports by the subjects of SL and TST. There was a significant increase in TST as assessed by PSG between baseline and post-treatment values for the active treatment group (76.0 +/- 11.1 minutes, p = 0.0001). The increase for the inactive treatment group was not statistically significant. The TST improvement was significantly greater for the active group when compared to the inactive group (adjusted for baseline TST; p = 0.020. R1 = 0.20). There was a significant decrease in SL as assessed by PSG between baseline and post-treatment values for the active treatment group (-21.6 +/- 5.9 minutes, p = 0.0006), whereas the decrease noted for the inactive treatment group was not statistically significant. The difference in SL decrease between the two treatment groups was marginally significant (adjusted for baseline SL and center, p = 0.068, R2 = 0.60). The number of sleep cycles per night increased by 30% after active treatment (p = 0.0001) but was unchanged following inactive treatment. Subjects did not experience rebound insomnia, and there were no significant side effects. The data presented in this report indicate that LEET administered for 20 minutes three times a week increased TST and reduced SL in chronic psychophysiological insomnia. LEET is safe and well tolerated and it effectively improved the sleep of chronic insomniacs given 12 treatments over a 4-week period by increasing the number of sleep cycles without altering the percentage of the various sleep stages during the night. The therapeutic action of LEET differs from that of currently available drug therapies in that the sleep pattern noted in insomniacs following LEET treatment more closely resembles nocturnal physiological sleep. This novel treatment may offer an attractive alternative therapy for chronic insomnia.

Bright light and LEET effects on circadian rhythms, sleep and cognitive performance.

Shift work and jet lag can disrupt cicadian rhythms, with detrimetnal effects on alertness, performance and sleep. This study examined the effects of two interventions to adapt circadian rhythms, sleep and performance to a 10-h phase delay of the work-rest cycle. Bright light was administered from 2200 to 0200 each night to promote phase delay of circadian rhythms. Low energy emission therapy (LEET) was administered for 20 min prior to daytime sleep periods to promote sleep. Twelve subjects received bright light, 12 subjects received LEET, 11 received both interventions and 10 control subjects received only placebo treatments. Bright light accelerated phase delay of the circadian melatonin rhythms after the work-rest schedule shift. Further, subjects who received bright light had greater total sleep time (TST) and improved sleep continuity. LEET treatment produced a trend (p = 0.16) for increased TST, but LEET did not affect the melatonin circadian rhythm. After the schedule shift, cognitive performance measures showed few significant differences. Some minor improvements in cognitive performance were producced by light treatments but not by LEET.

Electroencephalographic changes following low energy emission therapy.

Low energy emission therapy (LEET) is a novel approach to delivering low levels of amplitude-modulated electromagnetic fields to the human brain. The sleep electroencephalogram (EEG) effects of a 15-min LEET treatment were investigated in a double-find cross-over study to assess sleep induction. Fifty-two healthy volunteers were exposed to both active and inactive LEET treatment sessions, with a minimum interval of 1 week between the two sessions. Baseline EEGs were obtained, and 15-min posttreatment EEGs were recorded and analyzed according to the Loomis classification. A significant increase in the duration of stage B1 sleep (0.58 +/- 2.42 min [mean +/- SD], p = 0.046), decreased latency to the first 10 sec epoch of sleep (-1.23 +/- 5.32 min, p = 0.051) and decreased latency to sleep stage B2 (-1.21 +/- 5.25 min, p = 0.052) were observed after active treatment. Additionally, establishment of slow waves with progression from stages B to C was significantly more pronounced after active LEET treatment (p = 0.040). A combined analysis of these results with those of an identical study performed in Denver showed that LEET had a significant effect on afternoon sleep induction and maintenance with shorter sleep latencies (decreased latency to the first 10 sec epoch of sleep; -1.00 +/- 5.51 min, p = 0.033; decreased latency to sleep stage B2; -1.49 +/- 5.40 min, p = 0.003), an increased duration of stage B2 (0.67 +/- 2.50 min, p = 0.003), an increase in the total duration of sleep (0.69 +/- 4.21 min, p = 0.049), and a more prominent establishment of slow waves with progression to a deeper sleep stage (p = 0.006). It is concluded that the intermittent 42.7 HZ amplitude modulation of 27.12-MHz electromagnetic fields results in EEG changes consistent with shorter sleep latencies, longer sleep duration, and deeper sleep in healthy subjects.

Sleep inducing effect of low energy emission therapy.

The sleep inducing effect of a 15 min treatment with either an active or an inactive Low Energy Emission Therapy (LEET) device emitting amplitude-modulated electromagnetic (EM) fields was investigated in a double-blind cross-over study performed on 52 healthy subjects. All subjects were exposed to both active and inactive LEET treatment sessions, with an interval of at least 1 week between the two sessions. LEET consists of 27.12 MHz amplitude-modulated (sine wave) EM fields emitted intrabuccally by means of an electrically conducting mouthpiece in direct contact with the oral mucosa. The estimated local peak SAR is less than 10 W/kg in the oral mucosa and 0.1 to 100 mW/kg in brain tissue. No appreciable sensation is experienced during treatment, and subjects are therefore unable to tell whether they are receiving an active or an inactive treatment. In this study the active treatment consisted of EM fields intermittently amplitude-modulated (sine wave) at 42.7 Hz for 3 s followed by a pause of 1 s during which no EM fields were emitted. During the inactive treatment no EM fields were emitted. Baseline EEGs were obtained and 15 min post-treatment EEGs were recorded and analyzed according to the Loomis classification. A significant decrease (paired t test) in sleep latency to stage B2 (-1.78 +/- 5.57 min, P = 0.013), and an increase in the total duration of stage B2 (1.15 +/- 2.47 min, P = 0.0008) were observed on active treatment as compared with inactive treatment.(ABSTRACT TRUNCATED AT 250 WORDS)