The Starfish Project

The combined effort of our whole family.

Posts Tagged ‘alternative cancer treatment

Update on Mom (5/19/09)

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Last Friday, Mom’s hand started hurting quite a bit and three of her fingers started getting purple.  After the incident with her thumb, we knew what that meant.  So, Dad and Gretchen loaded Mom up and took her back to the ER.  They saw the same ER doctor we saw last time (which was helpful, as he was already familiar with Mom).  He couldn’t find a clot with the doplar, but felt they were probably small clots that were down in the capillaries of her fingers.  He wrote them a prescription for some nitro glycerine ointment which had to be applied to her hand every few hours and wrapped up.  This ointment is such a strong vasodialater that the person applying it had to wear gloves and be careful not to let their skin come into contact with it.  He said to use this through the weekend and if it didn’t help by Monday, to get Mom in to see a hand doctor.

Dad faithfully applied the ointment all weekend and Mom’s hand was still hurting quite a bit – so much that she needed to take pain pills to take the edge off the pain.  From what I’ve read, the pain from circulation problems caused by blood clots is quite terrible.  Mom and Dad had a pretty rough weekend with it with very little sleep.

On Monday morning, Gretchen started bombarding the primary care doctor’s office with requests for a referral to a hand specialist ASAP.  They were right on the ball and Mom had an appointment for 11:00 AM this morning.

I am still recovering from the flu (the normal one), so I still haven’t seen Mom since the morning of the 15th.  So, Dad and Gretchen took Mom over to the hand doctor this morning.  He did an x-ray and found that the clot was further up her arm, near her armpit.  The doctor was respectful, but still didn’t have any good news either.  He looked at Mom’s three fingers (which were now purple) and said that she would lose them, as well as the index finger and the rest of her hand.  He said all we could do was make her comfortable until all this happened and he could amputate her right hand.  He gave her a prescription for Darvocette and sent her on her way.

Well, this was definitely not the kind of news we wanted to hear.  But, we’ve learned that allopathic doctors generally don’t have good news for us (except for a few who we’ve appreciated so much).

Gretchen called me when they got home from the doctor and she was pretty shook up.  I imagine all three of them were – especially Mom.  I was also pretty shook up too.  I asked Gretchen how long she was going to be at Mom and Dad’s house and she said she was going to be there for a few more hours.

I got on the internet and started looking for anything that looked like it might work.  After only about 30 minutes of searching, I was amazed to find information about a supplement called Nattokinase.  It is an enzyme that aids in breaking up fibrin (a strand-like portion of the blood) that forms blockages in veins.  The Nattokinase is derived from fermented soybeans and has long been used in Japan to deal with and/or prevent blood clots.  It comes in a standardized formula which Gretchen was able to purchase at the health food store for around $30 (but available MUCH cheaper online through VitaCost for less than $7).  But, we needed it today, so Gretchen paid the $30 for it today.

She also picked up some stuff to make a blood thinning soup — it consisted of an organic beef broth base, onions, garlic, and green cabbage.  All of these veggies are good for naturally thinning the blood in both the arteries and the veins.

So, at 4:00 PM tonight, Mom was hurting, a bit scared, but encouraged that we had possibly found a solution that would save her hand.  She took her first 2,000 FU Nattokinase pill.  Gretchen also made the soup and Mom scarfed down a good portion of that too.  And, then we waited…

Gretchen came home (where I was babysitting her kids) at around 9:30 PM, and she said that you could already see a difference in Mom’s fingers.  She said that all day today the three fingers had a very delineated purple line straight across where the circulation was being compromised.  But, only 5 1/2 hours after taking the Nattokinase, the lines were no longer straight and it was now blotchy (with areas of pink) where they had once been only purple.

Gretchen called back at Midnight to remind Dad to give Mom her next dose of the Nattokinase and he said he had just given it to her.  But, then came THE BEST NEWS —- Mom’s hand no longer hurt.  She was sleeping and in absolutely no pain!!!  She hadn’t taken a pain pill since the morning and her hand was no longer hurting.  It had been hurting terribly since last week – but, the pain is now gone.  Gretchen asked if it was still purple, but he said they were in bed and the light was off and he didn’t know.  But, since the pain was gone, that can only mean that the circulation has been restored to her fingers and hand.  Isn’t that just awesome?

The thing that we have come to realize in this journey with cancer is that we, as a family, are alone.  We can’t count on my Mom’s doctors to know what to do anymore because they just simply don’t know what to do anymore.  Perhaps the insurance company doesn’t want to pay for any more treatment for her because they’ve now classified her as “terminal.”  Who knows.  But, perhaps it’s the best thing that could have happened to us.  Because, we’re finding that there are answers out there for many of the things that conventional medicine says are hopeless.

Mom has been taking her Poly-MVA now consistently for a few days and her appetite is returning.  Tonight is the first time in several weeks that she hasn’t had some kind of pain or another.  We’re praising God about that.  He’s been with our family through all of this and showing us that His ways are higher than our ways — His thoughts are higher than our thoughts.

Well, it’s very late and I need to get to bed.  Thank you to everyone (both those we know and those we don’t) who’ve whispered a prayer to heaven on Mom’s behalf.  We know we’re not really alone.  But, sometimes it feels like it.

Until next time (I’ll try to update tomorrow on the status of Mom’s fingers and hand) …



Low Dose Naltrexone (LDN) for Cancer Treatment

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naltrexoneIn Brief

Although prospective, controlled clinical trials on LDN in the treatment of cancer are yet to be accomplished, as of March 2004 clinical “off-label” use of this medication by Dr. Bihari in some 450 patients with cancer — almost all of whom had failed to respond to standard treatments — suggests that more than 60% of patients with cancer may significantly benefit from LDN.

Of the 354 patients with whom Dr. Bihari had regular follow-up, 86 have shown objective signs of significant tumor shrinkage, at least a 75% reduction. 125 patients have stabilized and/or are moving toward remission.

Dr. Bihari’s results sharply contrast to prior usual cancer treatment outcomes: either a cancer-induced death or a total cure. LDN therapy presents a viable third alternative, the possible long-term stabilization and/or gradual reduction of tumor mass volume.

Thus, with LDN, cancer can — in some cases — become a manageable chronic disease. Patients have the possibility of living free of symptoms, without, in many cases, the crippling side-effects of chemotherapy and radiation treatment.

> How It Works

Low dose naltrexone might exert its effects on tumor growth through a mix of three possible mechanisms:

  1. By inducing increases of metenkephalin (an endorphin produced in large amounts in the adrenal medulla) and beta endorphin in the blood stream;
  2. By inducing an increase in the number and density of opiate receptors on the tumor cell membranes, thereby making them more responsive to the growth-inhibiting effects of the already-present levels of endorphins, which induce apoptosis (cell death) in the cancer cells; and
  3. By increasing the natural killer (NK) cell numbers and NK cell activity and lymphocyte activated CD8 numbers, which are quite responsive to increased levels of endorphins.

> Cancers that are reported by Dr. Bihari to apparently respond to LDN:

  • Bladder Cancer
  • Breast Cancer
  • Carcinoid
  • Colon & Rectal Cancer
  • Glioblastoma
  • Liver Cancer
  • Lung Cancer (Non-Small Cell)
  • Lymphocytic Leukemia (chronic)
  • Lymphoma (Hodgkin’s and Non-Hodgkin’s)
  • Malignant Melanoma
  • Multiple Myeloma
  • Neuroblastoma
  • Ovarian Cancer
  • Pancreatic Cancer
  • Prostate Cancer (untreated)
  • Renal Cell Carcinoma
  • Throat Cancer
  • Uterine Cancer

> What the Future Holds

If the results of trials of low dose naltrexone in certain cancers are positive, the drug could eventually become an additional mainstay of cancer treatment — adjunctive with chemotherapy, radiation, and other cancer cell growth inhibitor receptor agonists — or even a replacement for current therapies, as primary treatment for those cancers that show little response to standard therapies.

> As of March 2004

Since February 1999, Dr. Bihari has begun treatment of some 450 cancer patients with LDN. Since many of these patients, particularly those seen before October 2000, were seen only once in consultation with medical follow-up by their oncologists, Dr. Bihari is missing up-to-date follow-up data on 96 patients.

As of March 2004, of the remaining 354 patients, 84 have died, all but 4 of cancer-related causes. Most of these deaths have occurred in the first 8 to 12 weeks on LDN. For the most part, these were patients who were quite ill when first seen, and had exhausted all other treatment possibilities. Of the remaining 270 patients, 220 have been on LDN for six months or longer. Of these, 86 have shown significant movement toward remission, identified for this purpose as a reduction of at least 75% in tumor mass and tumor-related symptoms. Of the other 134 patients, 9 have continued to show tumor progression, whereas the other 125 have stabilized and/or are moving toward remission but do not yet meet the 75% reduction criterion.


Among those who have shown significant movement toward remission, most had never received chemotherapy. The apparent remissions:

  • 2 children with neuroblastoma
  • 6 patients with non-Hodgkin’s lymphoma
  • 3 with Hodgkin’s disease
  • 5 with pancreatic cancer metastatic to the liver
  • 5 with multiple myeloma
  • 1 with carcinoid
  • 4 with breast cancer metastatic to bone
  • 4 with ovarian cancer
  • 18 with non-small cell cancer of the lung
  • 1 with small cell cancer of the lung
  • 5 with prostate cancer (no prior hormone-blocking therapy)(Although recently-diagnosed prostate cancer patients who have not received other therapies appear to do well on LDN, patients with prostate cancer who have already been treated with hormone-related therapies, including testosterone-blocking drugs and PC-Spes, have not responded to LDN.)

An overview of these results must assume the basic statistical principle that the patients with no follow-up contact have not done as well as those who have maintained continual medical contact with Dr. Bihari. Measured in terms of disease stabilization and/or movement toward remission, and assuming that patients in continual follow-up are twice as likely to have had a good outcome thus far, it appears that over one-half of all cancer patients whom Dr. Bihari has started on LDN have done well.

Taking into account the relatively large number of patients who were in advanced stages of disease when first seen by Dr. Bihari, and that some patients in the “not followed up” and “LDN < 6 mos” groups will likely have positive outcomes, it appears possible that more than 60% of patients with cancer may significantly benefit from LDN. This is underscored by Dr. Bihari’s observation that better outcomes tend to be seen when treatment with LDN is begun in earlier stages of the disease. Of interest, there is a negligible rate of relapse in patients who are started on LDN after or during successful initial treatment with surgery (e.g., for breast cancer) or with chemotherapy (e.g., for Hodgkin’s disease or non-Hodgkin’s lymphoma).

It will clearly require extensive study of LDN in prospective, controlled clinical trials to determine which cancers respond best and which other therapies are complementary to or synergistic with LDN.

> Other Developments

LDN Alone in the Treatment of Cancer. Dr. Bihari now has 88 patients with cancer in complete or partial remission whose improvement appears to be clearly attributable to LDN alone. In contrast, the vast majority of patients who consult with him for cancer tend to be on other concurrent treatments as well, which obviously interferes with drawing conclusions about LDN’s role in their improvement. The successful LDN-only group includes five breast cancer patients, one patient who had widespread metastatic renal cell carcinoma, three with Hodgkin’s disease and six with non-Hodgkin’s lymphoma. Other such cases, some now on LDN for as long as four years, include a score of patients with non-small cell lung cancer, as well as patients with ovarian cancer, uterine cancer, pancreatic cancer (treated early), untreated prostate cancer, colon cancer, malignant melanoma, throat cancer, primary liver cancer, chronic lymphocytic leukemia, multiple myeloma and some others.

NCI Examining LDN Cancer Cases. In June 2002 an oncologist and an oncology physician’s assistant from the National Cancer Institute reviewed some 30 charts of cancer patients at Dr. Bihari’s office. About half were chosen as appearing to have responded to LDN without question. With patients’ permission, copies of these were sent to the NCI for further data collection on its part for consideration for NCI’s Best Case Series.

Noteworthy Cases




> As of June 2004

Lung Cancer. C., a 61 year old woman, previously a heavy smoker, was found to have a lesion in the right upper lobe of the lung in 1999 and a supraclavicular node in April 2001. Biopsy showed that the node was metastatic from the lung tumor. In August 2001 an MRI of the chest showed supraclavicular clusters of nodes and stellate-shaped lesions in the apex of the right upper lobe. She then started taking low dose naltrexone. She began getting quarterly C-T scans of the chest, which have shown no change over the following 40 months. The C-T scan interval was changed to every 6 months. Her most recent C-T scan in the spring of 2004 continues to show no change from the August 2001 films.

Malignant Melanoma. L. is a 53 year old woman with metastatic malignant melanoma whom Dr. Bihari first saw in August 2000. Her primary skin lesion had been removed from the lower back in late 1976. A lump in the left groin was biopsy positive in December 1977. It appeared to respond to treatment with BCG in a clinical trial in January 1978. She was disease free for 20 years until a cancerous lesion appeared near the site of the original primary. It was removed surgically. She started a melanoma vaccine trial in April 1999 but developed two new skin lesions on the low back over the next six months. In February 2000 a bone scan showed a lesion in the left sixth thoracic rib, with growth evident on a repeat bone scan in April 2000, which also showed further lesions in the left sacrum and the L5 vertebra. She began taking low dose naltrexone in August 2000. She showed no growth of these three bone lesions and no appearance of new lesions over a forty month period since that time. She has remained on naltrexone only.

Esophageal Cancer. Reverend X is a patient at John’s Hopkins Hospital where he received most of his medical care. He first developed problems with digestion and some pain in the mid-chest area with swallowing in April 2002. An upper GI exam in May 2002 showed narrowing and irregularity of the lower esophagus. In June 2002, a C-T scan of the chest, abdomen and pelvis showed a 2cm thickening of the lower esophagus extending into the upper stomach. Also seen were five enlarged nodes in the chest and five in the abdomen. Rev X refused chemotherapy and began low dose naltrexone in August 2002. In the following months his difficulty in swallowing has significantly decreased and his weight has stabilized. He notes an improved sense of well being. He has had no therapy but low dose naltrexone.

Renal Cell Carcinoma. R., a 41-year-old man from Toronto with renal cell carcinoma, with metastatic lesions in his liver and lungs, contacted Dr. Bihari about 36 months ago. His oncologists told him there was no effective therapy available, and he said he was anxious to try treatment with LDN. There was no further contact with the patient until early 2002 when his wife called to thank Dr. Bihari. She said that he was doing quite well and that there had been complete clearing of the metastatic lesions as demonstrated by chest and abdominal CT scans.

Throat Cancer. D., a 54-year-old man who had cancer of the tonsillar area in his throat along with two large metastatic lesions easily visible in his neck, had refused the extensive head and neck surgery proposed by his physicians. They held out little hope for him. Thirty months ago, Dr. Bihari prescribed LDN. The patient’s most recent contact with Dr. Bihari was in May 2004 when he was examined. The primary tumor had decreased by one-third in size and the two neck masses had regressed by about 50%. The patient had received no radiation or chemotherapy but had tried unproven alternative treatments obtained in Mexico.

Non-Hodgkin’s Lymphoma. B., a 75-year-old woman, was diagnosed with non-Hodgkin’s lymphoma in January 1999 by a biopsy of an enlarged lymph node in the side of her neck. CT scans showed enlarged nodes in her chest and abdomen, as well as an enlarged spleen. Bone marrow biopsy showed “10% involvement”. Her oncologist recommended a wait and watch approach. She started LDN in July 1999. In January 2000, CT of the chest showed an approximately 50% decrease in the size of all the involved nodes. Repeat CT of the chest in November 2000 showed an 80% decrease in total tumor mass.

Prostate Cancer. M. is a 59-year-old man with prostate cancer, diagnosed with a biopsy and CT scan in September 1999. With no treatment other than low dose naltrexone, after 4 months on LDN his PSA dropped from 6.3 to 3.4. A special ultrasound, performed after 6 months on LDN, showed a 65% shrinkage of the tumor. His PSA remained stable over the following 16 months when he became ill and died of what may have been a cerebrovascular accident.

Pancreatic Cancer. D. was an 82-year-old woman with pancreatic cancer, treated with surgical removal in April 1999. Scans showed that a tumor mass had reappeared in the pancreatic area in August 1999, and two metastatic lesions were noted in the liver at the same time. She started low dose naltrexone in September 1999 and stopped taking gemcytabine at that time after a short course of four weeks. Some four months thereafter, an MRI demonstrated disappearance of the primary tumor that had previously re-grown, and the liver metastases had cleared entirely. Two months later, D. had a heart attack and died.

Carcinoid. C. is a 53-year-old woman with carcinoid, a malignancy that generally arises in the appendix or small intestine and spreads to the bones and throughout the abdominal cavity. She started LDN in June 1999. At that time, she had considerable abdominal swelling, diarrhea two to three times a day, frequent episodes of flushing due to the tumor, poor energy and appetite, and significant metastatic spread to numerous bones. No other treatment for the cancer was administered; none was available. By December 1999, much of the cancer-induced swelling of the abdomen had receded, the diarrhea had completely stopped, the flushing had stopped, and the pain in her right elbow, due to a bony metastasis, had markedly decreased. Follow up in February 2001 indicated that she still had some of the above symptoms and, though clinically stable, was not showing further movement towards remission. A telephone follow-up call in April 2004 indicated that she was experiencing only minimal symptoms.

Multiple Myeloma. W. is a 72-year-old man with multiple myeloma, diagnosed in the summer of 1998 when a medical workup for severe back pain (that occurred while playing golf ) revealed fractures of three vertebrae. Tumor was present in several other bones, blood counts were low, and a bone marrow biopsy showed 20% replacement of normal marrow with myeloma cells. His serum paraproteins were very high, as they often are in people with myeloma, at 12.6 and with no response to high dose chemotherapy. He started LDN in January 1999 and continued intermittent chemotherapy until October 1999. Since then, he had no chemotherapy but remained on LDN daily. There was a gradual normalization of all of his blood counts, as well as a drop in his abnormal serum proteins from 12.6 to a normal level of 1.4. Bone scans showed continued slow healing of affected bones, and two bone marrow biopsies showed no sign of myeloma. He had deferred plans for a high-dose chemotherapy with stem cell transplant procedure which had been earlier, and had decided to “watch and wait” while continuing nightly LDN. He was back to playing golf and tennis regularly, but there has been no contact since early 2003.

Hodgkin’s Disease. H., a 36-year-old RN with Hodgkin’s disease, was diagnosed in October 1991 with fevers, multiple infections (including toxoplasmosis of the brain), and a positive lymph node biopsy. She had a brief remission of several months following treatment with antibiotics and chemotherapy. She refused repeat chemotherapy when tumor activity resumed, and she remained ill with fevers and many gradually growing tumor masses (externally and internally) over the next four years. She started LDN in June 1997. No other therapy was provided. By October 1997, her fevers had cleared, all of her external enlarged lymph nodes had shrunk to normal, and all of the enlarged nodes seen in the spring of 1997 on CT scans were gone. She was determined by her oncologist to be in remission. Since that time, she has moved, gotten married, and not returned repeated phone calls. A long term friend reported that she continues to do well except for some persistent memory loss (due to brain lesions associated with her toxoplasmosis). She has stayed on LDN since and, as of the last phone contact in October 2003, had had no sign of relapse.

Non-Hodgkin’s lymphoma. J., a 48-year-old man, had a CT scan in January 1999 because of low back pain after an auto accident. In addition to a bulging disc in his spine, the CT scan showed many enlarged abdominal lymph nodes. Biopsies of nodes in two locations were diagnostic of a non-Hodgkin’s lymphoma. The patient refused chemotherapy and treated himself with antioxidants and multiple nutritional supplements. He added low dose naltrexone in October 1999. A repeat CT scan in late January 2000 showed a significant reduction in the size of the pathological nodes, each being reduced in size by about one-third. A more recent CT scan in early August 2003 showed further shrinkage of the enlarged nodes, which were reduced to less than 50% of their original size. The reduction of tumor mass occurred in the absence of chemotherapy or other standard treatments, with low dose naltrexone his only pharmacologic therapeutic agent.

Breast Cancer. M. is a 41-year-old patient with breast cancer, diagnosed and treated elsewhere in 1998, whose course was complicated by a recurrence involving metastasis to the hip. Outpatient hospice services were sought. Her walking was so badly impaired that she had to be assisted by her friends on her first office visit to Dr. Bihari in June 2000 — at which time she began LDN.  She revisited his office in mid-October and reported that she not only was able to return to work but also was well enough to play tennis again. Repeat bone scan in October 2000 showed a 40% reduction in metastatic tumor mass. She then enrolled in an experimental chemotherapy trial at a major cancer treatment center in New York in December of 2001 and died of liver failure on the fourth day of the trial.

Non-small Cell Lung Cancer. M. is a patient in his late 50’s who first visited Dr. Bihari in June 2000. A chronic cigarette smoker, he was told in May 2000 that he had metastatic non-small cell lung cancer. Many abnormal opaque areas had been seen on his chest x-ray, and a biopsy performed on a sizable mass in his right neck had confirmed the diagnosis. He had refused chemotherapy.  On examination, he had a 3cm x 4cm x 2cm mass in his right neck. He was started on LDN in mid-June 2000 and, at the beginning of November, revisited Dr.Bihari for the first time. At that time, the patient reported that energy was better and his appetite was good. He had regained 15 pounds, and had returned to working full time. The volume of the neck mass appeared to have decreased by 50%. An MRI exam in November 2000 showed 80% shrinkage of the right neck mass and 20% shrinkage of the masses in both lungs. As of April 2004, the mass in his right neck remained halved in size, with no further growth of his pulmonary lesions.

Ovarian Carcinoma. V., a 49-year-old woman, first visited Dr. Bihari in early September 2000. She had a five-year history of ovarian carcinoma, with a persistently growing tumor despite repeated courses of chemotherapy and multiple debulking surgery. There was recent increased involvement of the descending colon with the disappearance of formed stools, and she was now experiencing vomiting. Hospitalization was under consideration. She had lost 15 pounds in the two weeks prior to her visit. She was started on LDN at that time, in addition to her existing low-dose Taxol therapy, and within ten days  the signs of large bowel obstruction had disappeared. In four weeks, a repeat CA 125 revealed that this tumor marker had dropped from 1600 to 87. Within the first week of November 2000, it was reported down to 42, and her gynecologic oncologist told her that, on abdominal-pelvic examination, he found no masses. She had regained some 25 pounds and felt “wonderful”. A repeat MRI showed no visible masses. In March 2001, the CA 125 had risen to 52, then 70, with no return of symptoms or of palpable masses on abdominal and pelvic exams. However, in October 2001 the abdominal masses recurred despite LDN and she died of metastatic cancer four months later.





Before it was first used to treat cancer, LDN had been in use in the treatment of HIV/AIDS. A double-blinded placebo-controlled trial in 1986 showed significant immune system protection from HIV in a group of patients given the active drug. The development of LDN was based on several biological facts. One was the fact that naltrexone, which had been licensed in 1984 as an adjunct in treating heroin addiction, has the ability to induce increases in the endorphin levels in the body. Another was the fact that endorphins are the primary supervisors or (homeostatic) regulators of the immune system, representing 90% of immune system hormonal control. Ninety percent of the day’s endorphins are produced by the pituitary and adrenal glands between 2a.m. and 4a.m.

Dr. Bihari and his colleagues then showed that endorphin blood levels averaged less than 25% of normal in people with AIDS. These facts all provided the background for the discovery of the value of LDN in HIV/AIDS. The nocturnal production of endorphins allowed Dr. Bihari and his colleagues to experiment with small doses of naltrexone taken at bedtime in order to jump-start endorphin production. They found that LDN increased endorphin production when taken at bedtime in doses of 1.5mg to 4.5mg. Doses lower than 1.5mg had no effect on endorphin production. Doses higher than 4.5mg produced no more of an endorphin boost, but did block endorphins for significantly longer, thereby reducing the benefit of increased endorphin levels.

During the course of the placebo-controlled trial of LDN in people with AIDS in 1986, a friend of Dr. Bihari’s (M.B.) called him when she discovered that she was experiencing an exacerbation of non-Hodgkin’s lymphoma which had gone into remission five years earlier after treatment with chemotherapy. Because of her awareness of the decreased likelihood of a long-term remission with a second round of chemotherapy, she called to ask if his AIDS drug might help her cancer. A recently published study of human lymphoma transplanted into mice suggested that it might. In this study, all of the mice in an untreated group died of lymphoma. A second group of mice was pre-treated with a single injection of beta-endorphin before the lymphoma transplant. Half of this second group did not get ill with lymphoma. The other half of these mice did, but with a much more slowly growing tumor and a much prolonged life span compared with that of the non-pre-treated group.

Dr. Bihari agreed to treat M.B. with LDN, and used the three golf-ball-sized tumors in her groin as markers of response. All three shrank and disappeared over the next six months. M.B. stayed on LDN and had no further exacerbations of her malignancy. She died six years later in her mid-seventies from her third heart attack.

Several months later, Dr. Bihari, while in Paris to present the LDN AIDS results at an International AIDS Conference, met a woman (C.P.) in her early forties who was quite ill with metastatic malignant melanoma. This had spread from a malignant mole on her arm to her brain, which showed four metastases on C-T scan. Her speech was slurred, her balance and handwriting impaired, and she suffered from headache and recent memory impairment. Her oncologist in Paris said the malignancy was untreatable, and believed that she had perhaps three to six months of life remaining. On his return to New York, Dr. Bihari shipped LDN to C.P.’s daughter, who started the patient on it. Nine months later, with all neurological signs and symptoms having cleared, C.P. had a repeat C-T scan that showed no residual tumor.

C.P. remained on LDN for the succeeding 12 years, stopping it without her family’s knowledge in late 1999. Until that time, she had remained in complete remission, without any recurrence of her malignancy. Eight or nine months after stopping LDN she developed nodules under her skin and began to cough up blood. A C-T scan of the chest showed multiple metastatic lesions. Biopsy of one of the subcutaneous nodules confirmed recurrence of malignant melanoma. Dr. Bihari shipped LDN to the patient’s family and she resumed it in early 2000. Eight months later, the nodules in the skin had cleared and a repeat C-T scan of the chest showed no residual tumor. She appears to be, once again, in remission.

Over the years encompassed by these two cases, 1986 to 1999, Dr. Bihari focused his research energy on the study of LDN’s effect on immune function and on immunological approaches to the treatment of HIV/AIDS. In 1999, however, conversations with three small pharmaceutical companies revealed some interest in the development of LDN, with a goal of getting FDA approval for immune-related diseases including cancer. With this development possibility, Dr. Bihari decided to revisit the potential value of treating cancer with LDN.

Dr. Bihari began an informal private-practice-based evaluation of the effects of LDN with a variety of types of cancer in February 1999. He had seen positive results with a small but growing number of patients with cancer during the preceding 14 years, while developing the drug as an immune modulator for HIV/AIDS. The drug was compounded by pharmacists in 3mg capsules and taken once a day at bedtime. Most patients have recently had their LDN dose increased to 4.5mg daily. It is nontoxic and has no side effects. Its only interaction with other drugs is with narcotics (such as morphine, Demerol and Percocet), which it briefly blocks.

> Mechanisms

The mechanisms involved in the apparent beneficial effect of LDN on cancer have three main elements. The first is the effect of LDN, when taken late at night, in inducing a sharp increase in pituitary and adrenal production of beta-endorphin and metenkephalin, respectively, in the pre-dawn hours, when 90% of the day’s manufacture of these hormones occurs. Most studies have shown that naltrexone induces a two to three-fold increase in production of metenkephalin, the endorphin that most specifically activates delta-opioid receptors, the primary endorphin-related anti-growth factor on cancer cells. The low dose of naltrexone, which in higher doses would block endorphin and enkephalin action on the receptor, is gone from the body in about three or four hours — whereas the elevated levels of endorphins and enkephalins persist all day.

The second step involved in the anti-cancer effect of these hormones results from direct activation of opioid receptors of cancer cells by the increased endorphins. If this activation occurs while the cell is dividing, it dies. In fact, relatively small concentrations of metenkephalin, when added to human pancreatic cancer cells or human colon cancer cells growing in the test tube, have been shown to kill both. The apparent mechanism of cell killing is called apoptosis (programmed cell death). This appears to be one of the mechanisms by which endorphins and enkephalins combat cancer.

A third element, which may play a major role in controlling cancer, involves the cells of the immune system, which is regulated/orchestrated to a great extent by endorphins. In particular, endorphins raise the circulating levels of natural killer cells and lymphocyte-activated CD-8 cells, the two immunological cell types that prevent cancer by killing cancer cells as they arise.

It should be emphasized that Dr. Bihari’s patients were all treated in a private practice setting without the scientific rigor of a prospective clinical trial. This precludes any scientific claims about the drug’s efficacy in treating any of the above-mentioned types of cancer. The results thus far do, however, raise the possibility that the manipulation of opioid receptors on cancer cells as anti-growth factors through the use of endorphins and endorphin-inducing opioid antagonists may eventually prove to have considerable merit, particularly in view of the many years of published, supportive laboratory research findings.

Those cancer cells that have opioid receptors on their cell membranes, and that may, therefore, respond to LDN, include all of those that arise from the gastrointestinal tract. This includes the mouth, esophagus,liver, pancreas, stomach, small intestine, colon and rectum. Lymph glands and the spleen have large numbers of opioid receptors, suggesting that Hodgkin’s disease, non-Hodgkin’s lymphoma, multiple myeloma and lymphocytic leukemia should respond to LDN. Other malignancies with sizable numbers of opioid receptors on their cell membranes include breast cancer, neuroblastoma, prostate cancer, malignant melanoma, renal cell carcinoma, glioblastoma, astrocytoma, endometrial cancer and small cell and large cell cancers of the lung.

> Research History

Ian Zagon, Ph.D., whose research group has done much of the basic animal work in the area of cancer treatment and endorphins, showed in 1981 in a mouse neuroblastoma model that very small doses (0.1 mg./kg) of naltrexone, given once a day, inhibit tumor growth, prolong survival in those mice that develop tumors and protect some mice from developing tumors altogether.

Zagon had hypothesized that the small daily doses of naltrexone work to enhance the endorphin-related protective effect against cancer in mice by increasing the number and density of opiate receptors on tumor cells. He hypothesized as well that the increase in endorphins known to be induced by naltrexone might play a part in the protective effect of the small daily dose by working directly on the tumors’ opiate receptors.

In 1996 and 1997, Zagon and his co-workers, reported on laboratory research using specially-bred mice that had no immune system (so-called “nude mice”). They transplanted, in separate experiments, human colon cancer and human pancreatic cancer into the animals and compared the growth of the cancer between those mice that received daily injections of metenkephalin and a control group that received placebo. In each experiment, metenkephalin acted as a negative regulator of tumorigenesis and was significantly able to suppress tumor appearance and growth in the treated group.

Of especial importance, in 1996 the same group of researchers demonstrated that by utilizing LDN to induce an intermittent blockade of opioid receptors in similar laboratory animals (nude mice), the growth of inoculated human colon cancer was markedly retarded. “At the time (10 days) when all control mice had tumors, 80% of the mice in the 0.1 mg/kg NTX group had no signs of neoplasia.” When measurements of metenkephalin plasma levels were made, the group that received LDN had metenkephalin levels that were elevated 2.5-fold compared with the control group. The researchers concluded that the results suggested “that daily intermittent opioid receptor blockade with NTX [low dose naltrexone] provokes the interaction of opioids and receptors in the interval following drug availability, with opioids serving to inhibit tumorigenicity of human colon cancer”.

New findings by Zagon and colleagues at The Pennsylvania State University in Hershey were published in the December 1999 issue of the journal Brain Research. They had identified the specific cell receptor for one of the endorphins, metenkephalin (the levels of which are increased by LDN). Zagon stated that the opioids act as growth inhibitors, as well as neurotransmitters, and that this feature has implications for cancer treatment. Metenkephalin is found in all tissues, and appears to be associated with cells undergoing renewal or proliferation. Zagon’s group was described as having mounted Phase I trials using metenkephalin in an attempt to control the growth of pancreatic cancer in humans. Pancreatic tumors appear to have low levels of the metenkephalin receptor. Low peptide [metenkephalin] or [opioid] receptor levels may exist in cancer cells in general since they want to stimulate their own growth, Zagon said.

Source:  Low Dose

Lung Cancer Cured With Papaya Leaves

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Payapa Tree (called "paw paw" in Australia)

Papaya Tree (not paw paw)

[NOTE:  It’s important to note that in Australia, they call the Papaya Tree the “paw paw” tree.  But, this isn’t the same tree that we know in North America as the Paw Paw tree – which typically grows in the eastern part of the United States.]

AN American discovery that paw paw leaves may cure cancer is old news for a Gold Coast bookie who was extolling the plant’s virtues 14 years ago.

Stan Sheldon, then 70, told the bulletin in May 1978 how he beat cancer by following an old Aboriginal recipe and drinking the extract of boiled pawpaw leaves.

In 1962 he was given five months to live when leading specialists found he had rapidly spreading cancer in both lungs,

But after two months of drinking his pawpaw ‘tea” the specialists were astonished to find all signs of his malignancy had disappeared.

Cancer researchers in the United States were reported yesterday to have isolated a chemical compound in the pawpaw tree which was claimed to be a million times stronger than the most widely used anti cancer drug, Adriamycin.

The anti cancer substance, soon to be tested by the US National Cancer Institute, was found throughout the pawpaw tree, but primarily in twigs and small branches.


The Sheldon treatment involved cramming as many paw-paw leaves and stems as possible into a saucepan before adding water. After boiling, the mixture was allowed to simmer for two hours before being drained off. Mr Sheldon drank about 200 ml of the unpleasant tasting brew three times a day. In addition, he took three teaspoons of raw molasses a day another tip from the Aboriginal pharmacopea.

Back in 1978, Mr Sheldon was able to produce medical documentation and letters from his amazed specialists to back up his story. But he refused to label the pawpaw treatment as a “miracle cure for cancer.

All I am doing is reporting events that have happened,” he said. He decided to go public after a woman cancer victim earlier told the Bulletin how she had lost faith in doctors and was drinking a daily brew made from paw paw leaves in an attempt to beat her disease.

Mr Sheldon cautioned against foregoing accepted and proven methods of cancer treatment in favour of a herbal treatment such as paw paw leaves. But he said a number of friends had subsequently beaten cancer after trying the paw-paw tea.

Source:  Middle Path

Paw Paw Offers Hope for Cancer

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Dr. McLaughlin

Dr. McLaughlin

The pawpaw tree is indigenous to several areas of North America. 

Some have theorized that it receives its name due to its similar appearance to the papaya fruit; however, the two fruits are totally unrelated.  Pawpaw is of the scientific family Annonaceae, which includes several unusual tropical fruits. 

There are about eight different species of pawpaw; however it is the species Asimina triloba that was used by Dr. Jerry McLaughlin in his research, and it is only this species that contains the special annonaceous acetogenins that have been shown to so powerful in fighting insects, cancer cells, parasites, lice, and other attackers.  The pawpaw is a cousin to the fruit known as graviola, but research has proven that although graviola has some similar natural chemical compounds, it is not as desirable or as powerful as Asimina triloba for medical use.  Unfortunately, however, some opportunistic companies will market graviola as an equal.   It is not.

 The trees themselves are not large as far as trees go.  Some are about the size of large shrubs, although many grow as high as 25 feet, and sometimes a little more.  The fruit itself is about the size of a large human fist–usually 3-6 inches long– and is considered by many to be very tasty.  It is often compared to a combination of some sort of banana, coconut, mango, and possibly others. One reason that it is not available too often in retail settings is that it spoils quickly after it is harvested.  However, those who are fortunate enough to find a ripe fruit on a tree and eat it fresh are usually rewarded with a very pleasant tasting experience.

The fruit is also highly nutritious–very rich in proteins, good fats, and complex carbohydrates.  It is normally ripe in the fall, usually in September.  The explorers Meriwether Lewis and William Clark were known to have survived on pawpaw for about a month during their famous exploratory trip.

As a child, Jerry McLaughlin ate the fruit and felt that there must be something biologically active.  As a Professor of Pharmacognosy at Purdue University, he spent over 20 years studying this fruit.  He discovered the presence of a natural chemical in the tree called an acetogenin.  An acetogenin is a long-chained, fatty acid substance with some very unique properties.  Over 400 of these compounds have been found in nature, many of them by researchers working with Dr. McLaughlin at Purdue University.  In other parts of the world, researchers have been looking for acetogenins in other fruits of the same family.  However, the double-ringed features of the powerful acetogenins in the Asimina triloba have not been found to date in those other fruits.

Interestingly enough, the acetogenins that are so powerful are not as plentiful in the fruit as in the twigs of the tree.  Also, Dr. McLaughlin found that the acetogenin levels peaked in the twigs during the month of May.  Just as important, he found the levels of acetogenins vary even by location of the Asimina triloba trees.  Some groves produce higher levels than others.  Thus, if someone is considering using pawpaw as a treatment, it is not only important to ensure that the product is from the Asimina triloba species of pawpaw, but also that the product is standardized–in other words, the manufacturer uses an extraction process for the acetogenins and ensures that a guaranteed set amount (standardized amount) of acetogenins is actually in the product.  At this point, only one manufacturer in the world has the capability of accomplishing this, partially because Dr. McLaughlin has licensed his patent and methodology to them.

Steven Horne of Tree of Light Publishing put out a handout about the only standardized pawpaw product available.  Good quick source of information.  Published in 2003, some of the information about the antioxidants is a little outdated since recent tests by the Josephine Ford Cancer Center in Detroit indicate that using antioxidants with pawpaw does not interfere with the pawpaw action.

Look What’s Hidden in the Paw Paw Tree Fruit

During World War II, when bananas were scarce, Jerry L. McLaughlin’s dad gave him some “Indiana bananas” — the custard-like fruit of Asimina triloba, better known as the pawpaw tree. Though only about 4 years old at the time, McLaughlin recalls, “I threw up and never forgot them.”

A pharmacognosist at Purdue University in West Lafayette, Ind., McLaughlin now searches for plants possessing natural medicinal properties. Based on his unforgettable encounter with the Indiana banana, he focused a few years ago on the pawpaw. After all, he notes, “parmacology is simply toxicology at a lower dose.” The result: He reports finding a family of biologically active compounds — acetogenins — “that’s very good against cancer, and also terrific at killing insects.”

A crude extract of pawpaw twigs killed brine shrimp at a concentration of just 0.04 parts per million (ppm)–well below the 70 ppm concentration of strychnine needed to elicit the same effect. One novel acetogenin his team isolated from the pawpaw extract — asimicin — also proved lethal to blowfly larvae, two-spotted spider mites, Mexican bean beetles, mosquito larvae, melon aphids, striped cucumber beetles and a nematode. McLaughlin expects that natural asimicin-based pesticides, for which he holds a patent, may be marketed within four or five years.

McLaughlin also subjected brine shrimp to extracts from the pawpaw’s relatives. He hit a lode with Annona bullata, a Cuban native closely related to the “custard apple.” From this plant he extracted two acetogenins with anticancer prospects. In tests conducted by a major pharmaceutical company, one of those acetogenins — bullatacin — proved 1 million times more potent than the common anticancer drug cisplatin in inhibiting the growth of human ovarian tumors transplanted into mice. The National Cancer Institute is currently testing his acetogenins in in vitro trials, he says.

The acetogenins’ mode of action differs from that of most anticancer drugs: Rather than killing a cell by scrambling its DNA, they starve the rapidly divinding cells of the ATP that fuels them. As a result, McLaughlin says, “I don’t think we’ll have to worry about these [acetogenins] ever causing cancer–as some anticancer agents do.”

“Nor do we have to rely on Cuba to get bullatacin, the most potent acetogenin,” McLaughlin notes. In the March JOURNAL OF NATURAL PRODUCTS, he and his co-workers will announce isolating bullatacin and six other biologically active acetogenins–including a new compound, trilobacin–from the common pawpaw. The report also shows that trilobacin exhibited high levels of growth suppression in cultured cells of some leukemias, small-cell lung cancer, colon cancer, melanoma, ovarian cancer and renal cancer.

If the pawpaw contains so many potentially toxic agents, how can anyone stomach its fruit? In moderation, McLaughlin observes, the ripe fruit can prove quite edible. But his team’s assays indicate that unripe fruits “are almost as toxic as the twigs — really potent.” And that makes sense, he suspects, “because nature wanted to discourage animals from eating it and spreading its seeds before the fruit was ripe.”

Source:  Paw Paw

Graviola & Paw Paw For Treating Cancer

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by R. Webster Kehr

How It Works

North American Paw Paw Tree

North American Paw Paw Tree

These products come from trees in the tropical areas of South and North America. They kill cancer cells as a minimum, but may have other affects on cancer. Paw Paw is known to work by blocking ATP production and thus reduce the voltage of the cancer cell to the point it falls apart (apoptosis or programmed cell death). Because Paw Paw and graviola are cousins, I assume that is also the way graviola works. They are also known to build the immunity system.


Graviola Tree and Paw Paw Tree

This is one of those treatments for cancer that is fairly new, meaning it has only recently found its way onto the internet. Nevertheless, there have been a lot of scientific studies on these two products. At the current time most of the articles for Graviola and cancer come from a single source – the Health Sciences Institute (see the links below), though there are a growing number of independent articles.

I recommend graviola on the basis of several scientific articles, several testimonials, and several comments by practitioners (mostly from Brazil), however, Paw Paw is actually stronger than graviola at treating cancer. Paw Paw is the more potent of the two because of its more sophisticated and larger molecular structures. Graviola is sometimes called “Brazilian Paw Paw,” which can cause some confusion.

Paw Paw is clearly more powerful than graviola when treating cancer, if the quality of the processing is comparable. However, I would take freshly cut graviola over bottled Paw Paw (but American’s can’t get freshly cut graviola). Graviola only has single ring compounds, while the Paw Paw’s acetogenins have several double ring compounds (e.g. bullatacin) which makes Paw Paw much more powerful.

Paw Paw works (and I assume graviola as well) by slowing down or stopping the production of ATP. This in turn lowers the voltage of the cell. For normal cells, there is plenty of ATP, thus lowering the level of ATP has no effect on the cell. However, with cancer cells, due to the way they create energy (by fermentation), ATP is far more critical.

When the ATP level, and the energy of the cell level, drops to a critical level the cell falls apart. The residual pieces of the dead cancer cell are called “lysing” and I assume are similiar to other apoptosis (programmed cell death) killed cells. If that is the case, then part of the lysing is literally “eaten” by other cells (called: phagocytosed).

However, because the cancer cells in a cancer patient are frequently clusted together, a large amount of lysing can be created within a cancer patient such that high levels of clustered lysing cannot be eaten by surrounding cells. Such a situation is especially dangerous for lung cancer patients and brain cancer patients where a clustered amount of lysing can be very dangerous.

Here is some technical information on graviola:


  • “The Annonaceous acetogenins discovered in graviola thus far include: annocatalin, annohexocin, annomonicin, annomontacin, annomuricatin A & B, annomuricin A thru E, annomutacin, annonacin, annonacinone, annopentocin A thru C, cis-annonacin, cis-corossolone, cohibin A thru D, corepoxylone, coronin, corossolin, corossolone, donhexocin, epomuricenin A & B, gigantetrocin, gigantetrocin A & B, gigantetrocinone, gigantetronenin, goniothalamicin, iso-annonacin, javoricin, montanacin, montecristin, muracin A thru G, muricapentocin, muricatalicin, muricatalin, muri-catenol, muricatetrocin A & B muricatin D, muricatocin A thru C muricin H, muricin I, muricoreacin, murihexocin 3, murihexocin A thru C, murihexol, murisolin, robustocin, rolliniastatin 1 & 2, saba-delin, solamin, uvariamicin I & IV, xylomaticin.

Graviola, like its cousin Paw Paw, is known to greatly enhace the effectiveness of another alternative cancer treatment – Protocel. However, generally it is recommended that Protocel not be taken with graviola or Paw Paw. There are exceptions, see my Protocel article for more information:
Protocel Article

Because of the similarity of Paw Paw and graviola to Protocel, there is no doubt in my mind that in order to maximize the effectiveness of these products, they should be taken in exactly the same way as Protocel. In other words, every 6 hours, EXACTLY – 24 hours a day.

I would strongly recommend studying the Protocel article linked to above for information that will help you take these products.

Paw Paw has been shown to kill multiple-drug resistant (MDR) cells, which result from someone taking chemotherapy. This is critical to understand because when a person on orthodox treatments comes out of remission into regression, a high percentage of their cancer cells are MDR cells. This would REQUIRE the use of Paw Paw to treat these patients.

Paw Paw is not toxic according to studies with beagles (dogs). It appears to be impossible to ‘overdose’, 32 capsules 4x/day were non toxic because it caused vomiting.

Paw Paw gravitates towards cells that use a lot of energy and then cuts off their energy supply. Since cancer cells use 10-17 times as much energy as a normal cell, Paw Paw acts on cancer cells. It is the same mechanism that made it so useful as a parasite cleanse and to kill hair lice.

It is also the reason that pregnant women should not take Paw Paw. Paw Paw could see some of the fast growing cells in the fetus as high energy cells. In addition, some of the cells in a fetus are very similar to cancer cells (i.e. the “trophoblastic” cells), so pregnant women should ALWAYS be careful what they take for cancer.

If no cancer, parasite, or other high energy users are available, Paw Paw may gravitate towards fast growing cells lining the digestive and intestinal system walls. This is why the main manufacturer, Nature’s Sunshine, strongly cautions against long term use for non-cancer patients. Some people with cancer have reported digestion distress such as nausea. For this reason it is recommended to take Paw Paw with food.


Warnings For Both Products

In the past, it was thought that the effectiveness of Paw Paw, like Protocel, was damaged by taking antioxidants with Paw Paw. However, new research has shown that this is not the case. I quote from an email I received:


  • “The head of NSP research, Dr. Bill Keller, provided Paw Paw with supporting products to a research oncologist and his laboratory to test with actual cultures. Several of Nature’s Sunshine strong antioxidants were also provided. The research personnel concluded overwhelmingly that there was no negative prevention of Paw Paw action as a result of the antioxidants.”
    email to CancerTutor

Important Note: The above email is not the end of the story. Nature’s Sunshine researchers are still looking into this issue because there are some antioxidants that DO increase ATP energy, which would conflict with the use of Paw Paw, graviola and Protocel. I will put the results of their research on this web site as soon as I get more information!!

Also, I do not know which antioxidants may conflict with graviola. If you buy graviola, check with the vendor for recommendations.

No one with Parkinsons Disease should take Paw Paw or graviola unless alkaloid-free preparations are used. There is also a possibility of allergic reactions in sensitive individuals.


Supercharging This Treatment

Paw Paw is generally considered stronger than graviola. This does not mean that graviola should not be used. Cat’s Claw and Ellagic Acid seem to be items that people like to combine with Graviola. However, if you take Cat’s Claw make sure you take a product like Samento, which is a TOA-free Cat’s Claw.

Source:  Cancer Tutor

Written by Tracey

November 18, 2008 at 5:44 am

My Husband’s Full Recovery From Lung Tumor Without Drugs, Radiation or Surgery

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by Shirley Lipschutz-Robinson

In 1996 my husband’s routine physical checkup at the VA hospital (veteran
administration) revealed a tumor in one of his lung. The doctors wanted to
perform a biopsy immediately to find out if the growth was malignant and
they were already talking about radiation and chemo “therapy”. From past
experience and knowledge, I knew that this was not the answer. These so
called “therapies” provide no hope for real cure. Biopsies are very
traumatic to the body and chemo/radiation are well known to destroy the
immune system.

Instead, I immediately began to treat my husband (Chuck) with Homeopathy,
raw vegetable juice, flaxseed oil, herbal formula in tincture/extract form
such as the Essiac formula, the Hoxsey formula, and Cat’s Claw extract.
(more info on natural cancer cure:

Since 1996 doctors have continued to monitor Chuck’s tumor with their CAT
scan and PET scan. The tests revealed that a small mass still remains in
his lung, but the doctors aren’t concerned about it because the tumor has
completely stopped growing and Chuck experiences none of the usual symptoms
associated with lung cancer. To this day he remains healthy and well.

Source:  CureZone

The Breuss Cancer Cure – by Rudolf Breuss

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breussOccasionally throughout history, there have been men and women who have risen up from seeming obscurity to challenge the precepts we consider unchallengeable, to investigate and discover, and to apply their new-found knowledge for the betterment of mankind, no matter what the personal cost – Rudolf Breuss was such a man.

Born in 1899 into an impoverished Austrian family, Rudolf Breuss had a desire to heal and to cure from a very early age. His eager young mind absorbed every snippet of knowledge he could lay his hands on, but an alcoholic father with five children to clothe and feed, ensured that Breuss would never gain the education he so desired. Undeterred, he educated himself by reading books and attending lectures whenever he could – a practise he maintained throughout his life.

Breuss was a passionate man who cared greatly for the health and well-being of all mankind, and was infatuated by the prospect of discovering an alternative cure for cancer and other serious diseases – to him it seemed an oxymoron that maiming an individual through surgery could possibly be considered a cure. He was quoted as saying “To my mind, healing means returning a malfunctioning human body to full unrestricted function, not to remove parts of it by operation or amputation.”

According to Breuss, protein was primarily responsible for nurturing cancer, regardless of the type or where it was in the body. His prescribed solution was to fast for 42 days to starve the cancer of protein. Throughout the fast, a juice cocktail made from organically-grown beetroot, carrot, Chinese radish, celeriac and potato was taken, to detoxify and cleanse the body, and to stimulate the patient’s disease-fighting capabilities. Herbal teas were also an essential part of Breuss’ treatment program, with a range of blends designed to target specific illnesses.

The results were staggering. Throughout his career Breuss received over 45,000 testimonials from people who had been cured of cancer, leukaemia and many other seemingly incurable diseases, through the Total Cancer Treatment. Despite this incredible success there were those in the medical world who wanted him stopped.

At age 81, he was taken to court and accused of being a fraud and a quack by the anti-cancer industry. Breuss’ defence attorney – himself a cancer sufferer cured by Breuss – presented a number of cured patients to testify that they would be dead without Breuss and his Total Cancer Treatment program. Their testimony so overwhelmingly supported Breuss’ claims, that he was acquitted on all counts.

Breuss passed away in 1991, aged 92, but he left a legacy that will remain with humanity until disease and sickness are no more. Today, Breuss’ work is acknowledged by medical practitioners and herbalists alike. His best selling book The Breuss Cancer Cure has been translated into 5 languages and has sold over 1 million copies worldwide, spreading his message of hope to every corner of the planet.

The Breuss Cancer Cure is essential reading for every family. It not only provides a proven solution to one of the most feared diseases on earth, but it gives you an amazing insight into exactly what cancer is and what you need to do to prevent it.

Source:  Hilde Hemmes Herbals

Written by Tracey

November 9, 2008 at 10:10 pm