23 June 2012

Cancer Treatment with Electromagnetic Fields Moving Into Mainstream Medicine


British Journal of Cancer (2012) 106, 241–242. doi:10.1038/bjc.2011.576 www.bjcancer.com
Published online 17 January 2012

Treating cancer with amplitude-modulated electromagnetic fields: a potential paradigm shift, again?
C F Blackman
Integrated Systems Toxicology Division (B-105-03), US Environmental Protection Agency, Research Triangle Park, NC 27711, USA
Correspondence: Dr CF Blackman, E-mail: Blackman.Carl@epa.gov

The Zimmerman et al (2012) study published here, coupled with the group's two preceding papers (Barbault et al, 2009; Costa et al, 2011), identify a potential modality for treating tumours at a dramatic reduction in trauma and cost. This set of clinical and explanatory laboratory results should be understood in the context of the history of research into the biological effects of electromagnetic fields (EMFs).

The most successful clinical application is the use of EMF to initiate fusion in fractured long bones that would not otherwise heal. Pulsed fields were designed to simulate the natural piezoelectric signals generated from bones under varying stress while walking (e.g., Bassett, 1985). There are also other reports that EMF can reduce pain and stimulate wound healing after surgery.

The group's two previous clinical reports were critical to the design of this new Zimmerman et al study. Barbault et al (2009) described how they obtained the specific frequencies for different tumour diagnoses, which are then used in the amplitude-modulated (AM)-EMF treatment of those patients to stabilise the disease beyond normal expectations. Costa et al (2011) reported surprising clinical benefits from using the specific AM-EMF signals to treat advanced hepatocellular carcinoma, stabilising the disease and even producing partial responses up to 58 months in a subset of the patients. Now Zimmerman et al have examined the growth rate of human tumour cell lines from liver and breast cancers along with normal cells from those tissues exposed to AM-EMF. Reduced growth rate was observed for tumour cells exposed to tissue-specific AM-EMF, but no change in growth rate in normal cells derived from the same tissue type, or in tumour or normal cells from the other tissue type. The growth rate inhibitory response was field-strength (SAR) and exposure-time dependent. In ancillary tests, they observed reduction in gene expression and increases in mitotic spindle dysfunction only for the AM-EMF exposure that reduced the cell growth rate.

The work of Zimmerman et al, Costa et al and Barbault et al was not done in a vacuum. More than 30 years ago, Suzanne Bawin working in Ross Adey's lab (Bawin et al, 1975), with independent replication by my group (Blackman et al, 1979), demonstrated that biological effects could be caused by certain AM frequencies on a carrier wave but not other frequencies, similar to the current work. Subsequent reports in the 1980s by several groups continued to support and extend the initial findings (Adey, 1992; Blackman, 1992). Read more ...

21 June 2012

Phase II and III Clinical Trials Approved by FDA for Cancer Treatment with Electromagnetic Frequencies



BUSINESS OVERVIEW
The Company is focused on the commercialization of its first oncology application: treatment of advanced hepatocellular carcinoma. It has completed a phase II study, which shows a high degree of effectiveness as well as excellent tolerability, even in previously treated patients with severely impaired liver function. The company has designed a phase III registration trial, which has been approved by the FDA and will be initiated upon funding. Following successful completion of the phase III registration trial, the company expects to file for FDA approval for the treatment of advanced hepatocellular carcinoma. In 2012, the Company plans to initiate a phase II trial for the treatment of advanced breast cancer.

PRODUCT OVERVIEW
The TheraBionic technology is based on a platform technology which has been used in the treatment of several hundreds of patients enrolled in clinical studies in the US and Europe. Since 2001 the two main developers of this technology, Boris Pasche and Alexandre Barbault, have developed novel proprietary biofeedback devices and methods, which allowed for the identification of tumor-specific frequencies. In collaboration with Dr. Niels Kuster, a leader in the field of bioelectromagnetics, they have designed and filed a patent for a novel device (OncoBionic P1), which delivers electromagnetic energy with markedly higher precision. Successful completion of a feasibility study in patients with advanced cancer as well as a phase II study in patients with advanced hepatocellular carcinoma conducted at the University of São Paulo in Brazil have paved the way for the registration trial. Given this treatment's superior tolerability and efficacy as compared with current anticancer therapie, TheraBionic is expected to rapidly become a leader first in the treatment of hepatocellular carcinoma, then in other tumor types.

Read more ...

TheraBionic Publications

Blackman, C.F.
Treating cancer with amplitude-modulated electromagnetic fields: a potential paradigm shift,
again?
British Journal of Cancer 2012, 106:241-241
http://www.nature.com/bjc/journal/v106/n2/full/bjc2011576a.html

Zimmerman, J., Pennison, M., Brezovich, I., Yi, N., Yang, C.T., Ramaker, R., Absher, D., Myers,
R.M., Kuster, N., Costa, F.P., Barbault, A., Pasche, B.
Cancer cell proliferation is inhibited by specific modulation frequencies      
British Journal of Cancer 2012, 106:307 – 313
http://www.nature.com/bjc/journal/v106/n2/full/bjc2011523a.html

Costa, F.P., Cosme de Oliveira, A., Meirelles Jr, R., Machado, M.C.C., Zanesco, T., Surjan, R.,
Chammas, M.C., de Souza Rocha, M., Morgan, D., Cantor, A., Ivan Brezovich, Niels Kuster,
Barbault, A., Pasche, B.
Treatment of advanced hepatocellular carcinoma with very low levels of amplitude-modulated
electromagnetic fields
British Journal of Cancer 2011, 105: 640-648
PMID 21829195
http://www.nature.com/bjc/journal/v105/n5/full/bjc2011292a.html

16 June 2012

Carcinogenesis: Preventing it with electronic medicine

Bacillus licheniformis in fungus-like form. Photo by Milton Wainwright
As medical research advances, the strategy of systematically eliminating cancer cells with electromagnetic frequencies is entering the mainstream. A recent clinical trial showed clearly that low voltage application of frequencies destroys cancer cells, although their approach would need significant modification to be fully effective. Clinical trials have begun and electromagnetic frequencies have been approved by the FDA to treat certain tumor types. A remarkable video by Bill Doyle shows frequencies disrupting growth of cancer cells.

There are several steps to  dealing with cancer cells:
1. Nutritional and lifestyle factors described elsewhere are critical
2. Eliminate the Rife BX BY complex
3. Eliminate the Gregory cancer virus
4. Eliminate parasites that promote tumor growth
5. Disrupt glucose metabolism of cancer cells
6. Eliminate viruses that cause malignant cells
7. Target specific malignant cells for elimination

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There is abundant epidemiological data from all over the world on cancer incidence for a wide variety of tumors in animal and human populations. My thesis advisor was Editor of the Journal of the National Cancer Institute in the late 1970s and early 1980s. He gave me a stack of over 300 papers from the medical journals with carcinogenesis dose reponse curves for many different species. All the curves looked different. He told me to explain why they were all different and he would give me a Ph.D. I then spent about 8 years doing supercomputer mathematical analysis of data on various types of cancer. The final data set I focused in on for publication was data from the Third National Cancer Survey which had complete coverage from many states in the U.S. and was the best available data at the time. My thesis advisor had led the survey and I had complete access to all data at the National Cancer Institute. The core model we developed is now the generally accepted model for carcinogensis. It was initially validated for colon cancer. See:
Sutherland, JV and Bailar, JC. The multihit model of carcinogenesis: etiologic implications for colon cancer. J Chronic Dis. 1984;37(6):465-80.

For most human cancers, the data clearly shows a four hit process. This can be visualized most clearly in skin tumors. An abnormal cell appears and begins dividing and creates a small patch on the skin. Within this lesion, a cell mutates, and you have a small patch growing within a patch. This happens a third time, then a fourth time. On the fourth genetic change, the cell breaks through the mechanisms that control proliferation and is malignant. It grows uncontrollably in a fifth phase, with the right promoting environment available, and can get into the bloodstream and migrate to other parts of the body causing metastases.

I have repeatedly seen the frequencies 2008 and 2127 appear in myself and others after eating certain food. I have been able to confirm that this has happened in most people who have eaten a specific meal. This is the BX and BY “virus” form of Rife’s organism. Today, this is not believed to be a virus and some think it is a mycoplasma. Recent DNA sequencing of organisms found in cancer cells showed them to be a fungus.

These organisms are clearly not a typical virus. They immediately go systemic throughout the entire body. And it originally took days of repeated treatment for long periods with the FSCAN and/or EM6+ to clear the body of them. With newer technologies they can be eliminate a lot faster.

However, more and more evidence is appearing that shows cancer cell frequencies are specific frequencies in a virus sequence. It appears that a virus disrupting the cellular machinery is one of the critical steps (but not the only step) that produces a tumor. Therefore, eliminating the relevant viruses is critical to prevent ongoing appearance of pre-malignant or malignant cells.

I have repeatedly seen non-malignant skin tumors grow quickly and in one case apparently become malignant in the presence of BX and BY. In the presence of this organism it is common to have tumors erupt in less than a day. This helps to explain an interesting aspect of my previous research in carcinogenesis. In some tumors, prostate for example, the data show that the first malignant cell appears 35 years before clinical diagnosis on the average. In a fast growing tumor like lung cancer, the first malignant cell appears about a year before clinical diagnosis. However, it is very common to see people go downhill extremely quickly after initial diagnosis. While some of this is undoubtedly due to the shock of the diagnosis and resultant depression of the immune system, it is aggrevated by the BX and BY virus. Much of conventional cancer treatment does not eliminate the virus and may even promote its growth.

So the BX and BY organisms are strong promoters of at least stage 3 (premalignant) and stage 4 (malignant) tumors and may even promote earlier stages. As indicated in the paper by Owens DM, Wei S, Smart RC. A multihit, multistage model of chemical carcinogenesis. Carcinogenesis, Vol. 20, No. 9, 1837-1844, September 1999, promotion of early phases of tumor initiation increases the cellular population at risk of mutating into a subsequent phase. This process happens so fast in the presence of BX and BY that I believe the Rife organisms are both promoters and mutagens.

The first approach to stopping proliferation of tumors must be to eradicate the BX and BY virus. Parasites also release substances that promote tumor growth so they must be eliminated as well. However, they are not as dangerous as BX and BY. I believe if everyone was monitored for BX and BY and the infection was eliminated immediately, we could significantly cut cancer incidence in the U.S., probably by more than 50%.

The fact that this information has been available for almost 100 years now shows how closed mindedness and suppression of innovation has compromised American medicine. This phenomenon has largely been driven by business interests, initially by a director of the AMA who was ultimately convicted of fraud and conspiracy for suppressing cancer therapies, and in more recent years by the pharmaceutical industry.

The tumors I have worked with (lung, cervix, skin, colon) have all had the presence of BX and BY which can be eliminated straight away. It is important to realize when targeting the BX and BY organisms with an electronic device that when you kill one strain, another strain proliferates and the frequency changes. These organisms have very stable frequencies around 2008 and 2127, however, and I have seen them deviate only by 3HZ at the most. It is important to eliminate all of them and you must have the exact frequency to 1HZ and this frequency may vary between 2003-2010 and 2125-2130. In recent years, the frequency set for BX BY has expanded to hundreds of frequencies.

Eliminating the BX and BY organism does not stop cells which have already reached stage 4 and are malignant. In fact, all malignant tumors will not show BX and BY present. They can continue to proliferate and metastasize without BX and BY. The best way to eliminate the malignant cells is to stop the ATP metabolism in these cells while leaving normal cells unaffected. This will prevent mitosis and the cancer cells will die a normal death without proliferating. This appears to be possible with frequencies in the 11,700,000 range. These frequencies also seem to stop mitosis of stage 3 cells as well. The data in the Gorgun paper shows how this is possible.

Gorgun SS. Studies on the Interaction Between Electromagnetic
Fields and Living Matter Neoplastic Cellular Culture. Frontier Perspectives 7:2:44-59, Fall 1998.

Stopping cellular mitosis requires the exact frequency. I have seen frequencies in the range 11,600,000 – 11,900,000HZ affect tumors. Different tumors of the same type (or perhaps cells in different stages) will have slightly different frequencies. Metastatic tumors will have different frequencies. They must all be eliminated systematically, one by one.

I believe that Rife was able to affect a “cure” in almost every case because his device running at 11,700,000 had enough variability and harmonics to stop mitosis in all relevant cells, even though their frequencies may have been slightly different. The curse of modern technology is that it is so precise, most people are unable to reproduce Rife’s work.

Richard Loyd had a machine some years ago that could treat directly at 11,700,000HZ. Most of us are not so lucky. I have found some success, however, in using the FSCAN to treat all the octaves of the exact frequencies in the FSCAN range from 10-3,000,000HZ. More recent FSCAN devices work in the 11-12MHZ range. Current frequency sets provided to Frequency Foundation subscribers go well over 30MHZ to target viral patterns in the bodies energy field. It will be difficult but not impossible, in my view, to stop all cellular mitosis using a Rife device that can only treat at less than 10,000HZ.

These comments represent a working hypothesis that has been successful in many cases and not as successful in rapidly growing tumors. It needs further research and new data may alter the working hypothesis. I present it so that others can take a look and see if they can produce the same results consistently.
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Further study on cancer organims:
What is the Rife BX BY virus?
More questions on the Rife BX BY virus
More on the Rife BX BY virus and bacillus licheniformis
Gregory cancer virus
Identifying and eliminating the "cancer germ"
Origins of contemporary theory of carcinogenesis

Carcinogenesis: A multihit, multistage phenomenon

The Current Issue

I have a working hypothesis for cancer induction for use in electronic medicine that builds on my Ph.D. thesis and subsequent research. The essence of this research can be found in:

Sutherland, Jeff and Bailar, John. The multihit model of carcinogenesis: etiologic implications for colon cancer. J Chronic Dis 1984;37(6):465-80.

While this work built on the research of many of the leading scientists earlier in the 20th century, it marked the beginning of a turning point in the conventional wisdom about carcinogenesis. This can be seen in more recent research, for example:

Owens DM, Wei S, Smart RC. A multihit, multistage model of chemical carcinogenesis. Carcinogenesis, Vol. 20, No. 9, 1837-1844, September 1999

Abstract: Carcinogenesis involves the accumulation of genetic changes within a single cell. Tumor promotion functions in the initial clonal expansion of an initiated cell but is generally not considered to influence later stages. To investigate whether tumor promotion can influence later stages of carcinogenesis we developed a two-hit 7,12-dimethylbenz[a]anthracene (D) protocol designed to enrich for keratinocytes that contain at least two D-induced genetic alterations. FVB/N mice were initiated with D and promoted with 12-O-tetradecanoylphorbol-13-acetate (T) or treated with acetone (A) vehicle for 6 weeks. At 7 weeks after the start of promotion, but before visible papilloma development, groups of mice were treated with a second dose of D or A and 1 week later T promotion was resumed. D/T/A/T mice developed 2.8 papillomas/mouse and D/A/D/T mice demonstrated an additive tumor response and developed 5.8 papillomas/mouse. Importantly, D/T/D/T mice developed 12.4 papillomas/mouse, thereby demonstrating a synergistic tumor response compared with D/A/D/T and D/T/A/T mice. D/T/D/T papillomas exhibited increases in suprabasal S phase cells and keratin 13 expression when compared with D/T/A/T papillomas. D/T/D/T mice developed squamous cell carcinomas (SCCs) 10 weeks earlier than D/T/A/T mice and demonstrated a 96% malignancy incidence and 1.71 SCC/mouse compared with D/T/A/T mice, which demonstrated a 28% malignancy incidence and 0.32 SCC/mouse. Greater than 90% of D/T/A/T and D/T/D/T papillomas and SCCs contained mutant Ha-ras, while a normal Ha-ras allele persisted in all cases, indicating that a gene other than the remaining normal allele of Ha-ras was a target gene for the second D hit. These data demonstrate that: (i) promotion between the first and second hits has a profound outcome on carcinogenesis, presumably by increasing the probability that a second hit will occur in a previously initiated cell; (ii) continued promotion after the second hit is required for full expression of malignancy; (iii) the classic initiation–promotion protocol can be extended to a multihit, multistage model.

Carcinogenesis: Treatment Depends on Understanding the Multistage Model


Responding to reader requests, I recently published a summary paper on my work on carcinogenesis on this site. The paper was based in part, on my Ph.D. thesis which was published (in short form) as:

The multihit model of carcinogenesis: etiologic implications for colon cancer.
Sutherland JV, Bailar JC 3rd.
J Chronic Dis. 1984;37(6):465-80.

Noting that this paper is the basis of current understanding of cancer induction, I mentioned that recent sequencing of the genome has simply given more weight to the basic hypotheses. A recently published paper replicates my previous work. In fact the coauthor was a reviewer of my earlier paper. The National Academy of Sciences provides access to full text of the article.

Multistage carcinogenesis and the incidence of colorectal cancer
E. Georg Luebeck* and Suresh H. Moolgavkar
Proceedings of the National Academy of Sciences 99:23:15095-15100, November 12, 2002

We use general multistage models to fit the age-specific incidence of colorectal cancers in the Surveillance, Epidemiology, and End Results registry, which covers 10% of the U.S. population, while simultaneously adjusting for birth cohort and calendar year effects. The incidence of colorectal cancers in the Surveillance, Epidemiology, and End Results registry is most consistent with a model positing two rare events followed by a high-frequency event in the conversion of a normal stem cell into an initiated cell that expands clonally to give rise to an adenomatous polyp. Only one more rare event appears to be necessary for malignant transformation. The two rare events involved in initiation are interpreted to represent the homozygous loss of adenomatous polyposis coli gene function. The subsequent transition of a preinitiated stem cell into an initiated cell capable of clonal expansion via symmetric division is predicted to occur with a frequency too high for a mutational event but may reflect a positional effect in colonic crypts. Our results suggest it is not necessary to invoke genomic instability to explain colorectal cancer incidence rates in human populations. Temporal trends in the incidence of colon cancer appear to be dominated by calendar year effects. The model also predicts that interventions, such as administration of nonsteroidal anti-inflammatory drugs, designed to decrease the growth rate of adenomatous polyps, are very efficient at lowering colon cancer risk substantially, even when begun later in life. By contrast, interventions that decrease the rate of mutations at the adenomatous polyposis coli locus are much less effective in reducing the risk of colon cancer.

14 June 2012

The Real Cost of Dental Mercury

Concorde East/West Spri - May 2012
Executive summary 

While its use has essentially been eliminated in many countries, dental amalgam is now being considered for a global phase-out in the ongoing mercury treaty negotiations and in the European Union (BIO 2012) because of significant environmental concerns.  The negative effects of mercury releases related to amalgam use are widely recognized in countries where its use has been prevalent: it is often the largest source of mercury in municipal wastewater as well as an increasing source of mercury air pollution from crematoria.  On the other hand, high-quality mercury-free alternatives have long been available.  While most  dental professionals charge lower prices for amalgam fillings than for mercury-free alternatives, this paper shows that when factoring in “external” environmental and societal costs, amalgam is a higher-priced dental material by far (Hylander and Goodsite 2006).  Ultimately, society pays for mercury releases related to amalgam use through additional pollution control costs, the loss of common (public-owned) resources, and the health effects associated with mercury releases and contamination (MPP 2008).

According to the United Nations Environment Programme, the use of mercury in tooth fillings represents some 10% of global mercury consumption,  thus being among the largest consumer uses of mercury in the world (AMAP/UNEP 2008).  In  the U.S., as demonstrated in this report, mercury use in dentistry amounts to over 32 tons annually, which is considerably more than some recent estimates. For comparison, in the European Union dental applications comprise the second largest use of mercury, amounting to some 20-25% of the annual consumption of mercury in the EU.  With something less than twice the population of the U.S., the EU use of mercury in dentistry is somewhat more than twice the U.S. consumption (BIO 2012).


'via Blog this'

Vitamin D: You need more than you think!


Recently at the Frontier Medical Insitute, my Vitamin D levels were determined to be low, despite taking 5000 units of Vitamin D3 once or twice a day. You need more than you think.

In addition, I no longer use sun screen in order to maximize Vitamin D creation, since frequencies can eliminate basal cell carcinomas and prevent them by eliminating precursor cells. Still, my Vitamin D was low. This problem is now part of mainstream medicine as even conventional physicians treating some family members are checking Vitamin D and prescribing it as needed.

Recent papers in the Journal of Leukocyte Biology describes the mechanisms by which low Vitamin D increases risk of infection.


Vitamin D levels diminish with age, increasing risk for colds and influenza - Naturalnews.com 14 Jun 2012

To perform the analysis and gather data for this study, researchers compared the changes in the blood levels of vitamin D among three groups of healthy subjects: youth (aged 20 to 30), middle-aged (aged 31 to 59), and elderly (aged 60 to 86). The scientists found decreased levels of vitamin D with aging, likely due to decreased exposure to the sun and a decline in the native ability of skin receptors to produce precursor levels of vitamin D, commonly found among individuals above the age of 40.

The research team found that the level of circulating vitamin D in the blood affected the toll-like receptor (TLR) expression measured on white blood cell lymphocytes and monocytes. Specifically, they found that the TRL most affected by a vitamin D insufficiency is TLR7, which regulates the immune response against viruses. In many geographic regions, limited sun exposure during darker winter months is closely associated with vitamin D deficiency and increased risk for colds and influenza outbreaks.

The lead study author, Dr. John Wherry concluded"This study shows that sunlight, or more precisely the lack of vitamin D could have a role in the seasonally higher rates of infection... since vitamin D supplements are inexpensive and generally safe, this is a really exciting discovery."It is best not to rely on sun exposure or dietary sources to obtain vitamin D. Most health-minded adults will want to supplement with an oil-based form of Vitamin D3 (experts recommend starting with 5000 IU per day), and test twice a year using the 25(OH)D blood test to confirm optimal levels above 50 ng/mL to achieve optimal protection against colds, flu, and many viral infection strains.

Learn more:http://www.naturalnews.com/036168_vitamin_D_flu_infections.html#ixzz1xkZqnioP

02 June 2012

Fukushima Radiation Frequencies Version 2.0



Fukushima Radiation Frequencies Version 2.0 has several updates that adjust frequencies based on hair analysis at the Frontier Medical Institute in Colorado. These are posted on Frequency Foundation subscribers site.

Bad or no data from the Japanese government has led citizens to take radiation monitoring into their own hands. See maps.safecast.org for latest information on radiation levels.

Those individuals with a Hadoscan in many parts of the world periodically see a radioactive complex in their system that includes uranium, copper, lead, DDT, hexochlorophenol, and castoreum. This causes both internal symptomology and external skin itching and lesions. This may be the cause of hair loss on Alaska Airlines crew members. A review of lesions on the skin of Alaska Airlines pilots identified a specific frequency in this series.

The most common frequencies for these radiation effects are available (there may be other isotopes of some of these elements). Drink plenty of water as these frequencies will flush materials out through your urinary tract.

The homeopathic remedy Carbo Vegitabilis 30C is recommended along with the radiation frequencies.