Tuesday, 20 January 2015



Is it possible to stop cancer spreading? 

If so, HOW?

We are told that 9 out of 10 people that die from cancer die from metastases...not the original primary tumour. 

Read on for some important facts...

Fact: Most people that die from cancer die because the cancer has spread. Therefore it seems obvious that this is the one thing that must be stopped...at all costs, if possible. The fact that it has been proven that this outcome can often be stopped....with a cheap natural (non toxic) treatment (nutritional therapy) should be great news for mankind. But not if this knowledge is covered up and subjected to a campaign to discredit its value with lies and half-truths.
Most cancer victims choose chemotherapy. 
Most cancer deaths (almost all) are due to metastases.
It follows that chemotherapy fails to stop cancer spreading in millions of cases!

Below I reveal a number of substances and approaches that can often halt cancer and even reverse it, even when all hope looks to be gone.

Cannabis compound stops spread of breast cancer: 

From CBC News

A compound of the marijuana plant may prevent aggressive breast cancers from spreading throughout the body, new research from the United States suggests.
A team of researchers at the California Pacific Medical Center Research Institute say cannabis compound CBD could provide a non-toxic alternative to chemotherapy for cancer treatments. Previous research has shown the compound can block human brain cancers, and recent lab experiments have shown it may be able to do the same for breast cancer.
"Right now we have a limited range of options in treating aggressive forms of cancer. Those treatments, such as chemotherapy, can be effective but they can also be extremely toxic and difficult for patients," said researcher Dr. Sean McAllister in a release. "This compound offers the hope of a non-toxic therapy that could achieve the same results without any of the painful side effects."
CBD works by blocking the activity ofgene Id-1, which is associated with metastasis— the spread of cancer cells away from the original tumor site. The compound does not share marijuana's psychoactive properties.
"We know that Id-1 is a key regulator of the spread of breast cancer," said senior author Dr. Pierre-Yves Desprez in arelease. "We also know that Id-1 has also been found at higher levels in other forms of cancer. So what is exciting about this study is that if CBD can inhibit Id-1 in breast cancer cells, then it may also prove effective at stopping the spread of cancer cells in other forms of the disease, such as colon and brain or prostate cancer."
Researchers stressed that they were not encouraging cancer patients to smoke pot, adding that it would be highly unlikely for patients to receive an effective concentration of the compound in that way.
The team's findings were published in the journal Molecular Cancer Therapeutics.

Hemp Oil:

The following presentation of RUN FROM THE CURE: The Rick Simpson Story was made possible by Rick Simpson and video producer Christian Laurette... made for free to teach YOU how to heal yourself of disease and illness using cannabinoids.

Another great natural substance that can halt matastases is PECTIN...

Pectin induces apoptosis in human prostate cancer cells: correlation of apoptotic function with pectin structure

Extract from study:

Cancer therapy is aimed at either the primary tumor or metastatic cells. Because of the differences in the response of primary and metastatic cancers, most therapies do not address both cancer types. Pectin, a natural plant polysaccharide present in all higher plant cell walls, and thus in all fruits and vegetables and in most plant derived foods, is a compound that appears to be able to inhibit cancer metastasis and primary tumor growth in multiple types of cancer in animals. Although pectins were initially recognized as compounds capable of inhibiting metastatic lesions (Heitman et al. 1992; Platt and Raz 1992; Pienta et al. 1995; Nangia-Makker et al. 2002), more recently, pectins have been shown to reduce primary tumor growth (Nangia-Makker et al. 2002). It has been suggested that the inhibitory effects of pectin on metastatic lesions in the lung are mediated through their binding to galectin-3 (a galactoside-binding lectin). Galectins are specific carbohydrate-binding proteins present on the surface of cancer cells. Galectins facilitate cell–cell interactions by binding to galactose-containing molecules on neighboring cancer cells. In human colon, stomach and thyroid cancers, the amount of galectin increased with the progression of cancer. Blocking galectin-3 expression in highly malignant human breast, papillary, and tongue carcinoma cells led to reversion of the transformed phenotype and suppression of tumor growth in nude mice (Honjo et al. 2000, 2001). It has been proposed that the pH-modified CP blocks binding of galectins, and thus, inhibits tumor cell–cell interactions. The potential impact of blocking galectin action includes inhibition of the aggregation of cancer cells to each other and to normal cells, thus inhibiting metastatic lesions. However, LNCaP cells do not express galectin-3 (Ellerhorst et al. 1999,2002; Califice et al. 2004; our unpublished observations), suggesting that the apoptotic effects of pectins reported here are due to mechanisms not mediated through galectin-3.

The major goals of the present research were two-fold: (i) to identify pectins that are capable of inducing death of prostate cancer cells and (ii) to determine the structure of the pectin that is responsible for such biological effects. Initial experiments demonstrated that among the pectins tested, only FPP induced apoptosis. The pH-modified CP, PeS, is similar to the modified CP that has been shown to inhibit metastatic lesions and to induce apoptosis in multiple myeloma cells (Chauhan et al. 2005). Significantly, PeS did not induce appreciable apoptosis in prostate cancer cells, agreeing with published data showing no cytotoxic effects of pH-modified pectin on prostate cancer cells and xenografts (Pienta et al. 1995). Thus, the main thrust of the present research was to characterize the structure–function relationships of the apoptotic pectin FPP. Most of the published reports on the anticancer effects of pectin utilized pectins that were modified by alterations in pH in an effort to fragment pectin structure to facilitate biological effects in the systems under study. This procedure, in addition to fragmenting the pectin, may affect the structure of the pectin and thus its function. FPP was not produced by pH treatment, but rather was produced by heating CP. We therefore utilized several methods to correlate the biological function of FPP with its structure and compared FPP structure with that of PeS and CP, which were not apoptotic.
As a first step, the size and glycosyl residue composition and linkage of the different pectins were compared. Our results did not show any significant differences between the glycosyl residue composition or linkages of FPP compared with PeS and CP, indicating that differences in apoptotic activity among the three pectin preparations were not due to differences in the major types of pectin present. Also, there was no correlation in the size of the pectins and their apoptotic activity. As pectins consist of HG and RG, we hypothesized that one or more of these polysaccharides in FPP was responsible for its apoptotic effects. However, experiments testing the apoptotic effects of HG, RG-I, and RG-II, indicated that these individual structural components were not by themselves responsible for the apoptosis-inducing activity of FPP. We therefore conclude that the apoptosis-inducing activity of FPP is related to some structural constituent not detected by the above analyses.
To further understand the structure–function relationship of apoptotic pectin, FPP was specifically fragmented using endopolygalacturonase (EPG), which cleaves HG at contiguous nonesterified GalA residues. The cleavage of FPP with EPG did not have a major effect on its apoptotic activity. Thus, two methods were used to remove ester linkages from FPP prior to EPG treatment and thereby, make FPP more susceptible to EPG cleavage: chemical deesterification by mild base treatment and specific enzymatic hydrolysis of methyl esters by treatment with pectinmethylesterase (PME). Chemical deesterification of FPP resulted in significant loss of apoptosis suggesting that a base-sensitive structure, such as an ester linkage, is necessary for the apoptotic activity of FPP. Since specific cleavage of methyl esters by PME did not destroy FPP's apoptosis inducing activity, linkages other than methyl esters are required for apoptotic activity. Furthermore, PAGE analysis of intact and treated FPP showed that a polymeric/oligomeric FPP structure containing a base-sensitive linkage, and/or the specific base-sensitive linkage itself, is required for the apoptotic activity of FPP. Taken together the results suggest that an ester-based (or related) cross-link in pectin is important for the apoptosis-inducing activity of FPP.
The incubation of FPP with a nonspecific protease, with endo-α1,5-arabinase or with RNAse prior to cell treatment (data not shown), did not significantly affect FPP's apoptosis-inducing ability, suggesting that the apoptotic response is not due to the presence of proteins, α1,5-arabinan, or RNA within the pectin preparation. Significantly, we have been successful in generating the apoptosis-inducing capability in CP by heat treatment, a critical step in the production of FPP from the mother pectin. This supports our conclusion that a specific pectin structure and/or pectin-containing linkage is responsible for inducing apoptosis. The question of whether the heat treatment of CP causes a covalent or noncovalent modification of CP structure that leads to the apoptotic activity remains to be determined.
In conclusion, we provide the first evidence that specific structural characteristics of pectin are responsible for inducing apoptosis in cancer cells. Our results demonstrate that different extraction protocols may alter the structure of pectin and can lead to differences in pectin's apoptosis-inducing activity. Further experiments to identify the specific apoptotic structure in pectin will enable us to generate the smallest fragment that is capable of inducing apoptosis. A detailed understanding of structure–function relationships of such a fragment may lead to effective anti-cancer therapy. This is of particular therapeutic significance, as we have demonstrated that manipulating the structure of pectin results in a compound that is capable of inducing apoptosis in both androgen-responsive and androgen-independent prostate cancer cells. http://glycob.oxfordjournals.org/content/17/8/805.full

This scientific information is somewhat complex and technical for the lay person. However there is good evidence that the pectins found in almost all fruits can be helpful.

New Modified Citrus Pectin Slows Cancer Progression and Stops Cancer Cells in Their Tracks...

Study Shows New Modified Citrus Pectin Works as Well as Chemo
Without Toxicity and Improves Quality of Life in Advanced Disease
Better Health Publishing report that many people with cancer could be helped by anew form of Modified Citrus Pectin (MCP) that may work as well as chemotherapy 
in advanced disease stages; yet without the dangerous toxicity. These published 
findings of new capabilities for MCP have the potential to revolutionize cancer 

Previous research with MCP has shown it to be effective in slowing
the progression, metastasis and angiogenesis of several types of
cancer. Now with further improvement in the modification process, more
of the effective substance can be utilized by the body. The first
human study described below was done with patients with late stage,
breast, prostate, colorectal, kidney, pleural or lung, cervix/uterine
cancer, liver, pharynx, pancreatic, stomach, melanoma and bile duct

   This landmark clinical trial was published in the peer-reviewed
journal Clinical Medicine: Oncology, where it showed a significant
improvement of quality of life and stabilization of disease for
patients with advanced solid tumors. The results of the landmark
advanced tumor study clearly demonstrate MCP's enhanced capabilities.

   "This is a very important breakthrough destined to help a lot of
people," said Dr. Isaac Eliaz, a prominent doctor of Integrative
Medicine and MCP researcher. "MCP may have the benefits similar to
chemotherapy in advanced cancers, but without the side effects. This
study sheds additional light on the potential benefits of MCP in
cancer prevention and treatment."

   A background report on the development of MCP in integrative
cancer healthcare is available through Better Health Publishing at the
following url: www.betterhealthpublishing.org/mcpreport

   MCP, a natural substance modified from the peel of citrus fruit
has been used during the past decade in integrative cancer therapy to
help keep aberrant cells from clustering and blocking the formation of
blood vessel attachment. The absorption into the blood stream is based
on the size and weight of its molecules.

   MCP molecules bind to receptors on cancerous cells, preventing
these cells from attaching to healthy tissue and blocking the
formation of blood vessels to feed the cancerous cells. Once this has
occurred, the cancer cells starve and die or are eliminated by the
immune system.

   In the past, the enzymatic modification process produced too much
total breakdown of the pectin molecules when it tried to achieve the
effective low molecular weight absorbable chains. The new MCP also
goes through an enzymatic process that reduces the pectin's molecular
size and modifies it to better control the amount of total breakdown
of the citrus pectin. These new developments led to an improved MCP,
lower in weight, which allows it to be more systemic, circulating
through the blood stream and allowing the body to absorb more of the
effective molecules.

   Treatment and Scientific Data of Study:

   The treatment in the advanced tumor and previous studies consisted
of the oral intake of five grams of MCP three times a day. One cycle
of therapy was defined as four weeks of treatment. Objectives were
clinical benefit (pain, functional performance, weight change),
safety, tumor response (RESIST criteria) and quality of life.

   The results proved very exciting. Forty-nine patients (between 36
and 82 years old) with various advanced solid tumors were enrolled.
Twenty-nine patients were evaluated for clinical benefit after two
cycles of treatment. All patients tolerated the therapy well without
any adverse effects. The results also demonstrated that after two
cycles of oral intake of MCP, 6/29, (20.7%) had an overall clinical
benefit with a stabilization or improvement of life quality. On intent
to treat basis 11/49 patients (22.5%) showed a stable disease after
two cycles and 12.3% had a SD for more than 24 weeks. One patient with
advanced and hormonal resistant prostate cancer had a 50% decrease in
PSA with significant improvement in his quality of life. Most of the
patients had improvements in their life quality as reflected in the
Karnofsky scores.

   The MCP used in the advanced tumor study is now commercially
available in the US. It's called PectaSol-C and distributed by
EcoNugenics, Santa Rosa, CA.

   About Better Health Publishing:

   Better Health Publishing, founded by Isaac Eliaz, M.D. is a
publishing house that focuses on the publication of key works
promoting health and wellness. The staff at Better Health Publishing
believes that a natural and efficacious lifestyle is the cornerstone
of a return to healthy and sustainable society. The works published by
BHP strive to promote this concept and disseminate to the public a
healthier choice. For more information on Dr. Eliaz, log onto
www.dreliaz.org. For a free report on MCP log onto

The above Modified Citrus Pectin is a very exciting substance (that I personally used myself when fighting cancer) which, - according to the book below, - works on cancer cells and frustrates their objective to grow and spread. I'm sure the above results could be greatly enhanced by including an aggressive anti-cancer diet, along with other key measures to maximise results.

Stage 4 cancer healed:

Published on Apr 16, 2015
In 2011, Candice-Marie Fox was diagnosed with thyroid cancer. After surgery and radiation, it spread to her lungs and elsewhere, making it stage IV cancer. She adopted a radical nutrition and lifestyle change and her body healed. There is also a much longer version of her story which you can watch here:

This is a wonderful insight into how the body can rally and reverse cancer naturally, given the right approach. This approach is not suggested for every or any particular case of cancer, but is an insight into the fact that radical change of diet and lifestyle can seriously impact cancer, despite the fact that surgery and radiotherapy had depleted her immune system, and managed to spread the cancer massively in a very short space of time. This approach obviously requires expert instruction, along with a well structured protocol that you follow to the letter..

 Nutritional Oncology Research Institute (NORI)

The science of how a fruit based diet helps to kill off cancer cells.

Published on Apr 18, 2015
Mark Simon, founder of the Nutritional Oncology Research Institute, explains the NORI Protocol and how a high-fruit vegan diet can stop and reverse cancer growth.

Show notes athttp://www.chrisbeatcancer.com/how-a-...

NORI has researched and developed a unique approach to cancer therapy that is very simple, effective, low-cost, nontoxic and can be implemented at home.  It is based on targeting common metabolic abnormalities present in nearly all types of cancer cells.

A methionine restricted diet combined with a nontoxic chemotherapeutic cocktail is a unique and powerful approach to treating and managing malignancies.

An important feature of the NORI protocol is the
synergy created between the methionine restricted diet and high dose selenium.  Methionine restriction sensitizes cancer cells to sodium selenite by lowering glutathione which increases oxidative stress.  

The NORI approach is to leverage diet for maximum benefit while using a straightforward and highly targeted method for selectively killing cancer cells.

Cancer vanished!!! Starving cancer to death is one approach that worked for this guy, - who was given just a few more months to live!

Metabolic therapy works by starving cancer cells, (which require large amounts of GLUCOSE to survive) by avoiding all carbohydrates. Watch this short video to learn how it works, and about the results scientists are obtaining with this method.