The Work Continues: Two Cases of Metastatic Cancer Treated with an Enzyme-Based Nutritional Protocol


By Linda L. Isaacs, MD

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Since the death of my long-time colleague and friend, Nicholas Gonzalez, MD, I have continued to offer the same protocol that we used for patients with cancer and other degenerative diseases. The method is based on the work of William Donald Kelley, DDS; Nick had reviewed Kelley’s records and found many remarkable patient outcomes, as detailed in his book One Man Alone.1 Nick and I co-authored an article with 30 case reports in Alternative Therapies in Health and Medicine in 2007.2 At the time of his death, Nick was working on a collection of case reports from his practice and mine, which was subsequently published in two volumes.3,4

In a 2019 article, I reported the outcomes of two patients I first saw around the time of Nick’s death in 2015.5 Below, I provide an update of their status.


Patient 1: Metastatic Colon Cancer

Patient 1 had a right colectomy in May 2014, for a 4.5 cm adenocarcinoma with metastases in 2/32 lymph nodes. CT scan July 2014 showed three hepatic hemangiomas.

Instead of the recommended chemotherapy, Patient 1 followed a self-designed nutritional plan. CT December 2014 showed the three hepatic hemangiomas seen previously, and a low-attenuation lesion described as unchanged from previous exams.  PET scan was negative; but his CEA was steadily rising, so he began chemotherapy with FOLFOX.  CT scan June 2015 showed, in addition to the three hemangiomas, a new 0.8 x 0.9 cm low attenuation lesion in the liver. He discontinued chemotherapy at that time.

By December 2015, the liver lesion had grown to 1.7 x 1.5 cm. In February 2016, he underwent partial resection of the right lobe of the liver.  The pathology report stated: “Metastatic adenocarcinoma, consistent with colonic primary, extending focally to margin of resection.”

He began a nutritional program under my direction in April 2016.  Around the same time, a scan showed “Enlarging low attenuation lesion within the right lobe of the liver suspicious for metastatic disease.”

After two months on his protocol, abdominal CT showed a low attenuation hepatic mass, and CT of the chest showed a new “slight lobulated nodule … measuring 0.9 x 0.8 cm.” His oncologist strongly recommended resection of the lung nodule and the liver mass, as well as resumption of chemotherapy. However, Patient 1 told me that FOLFOX made him so sick that he would rather be dead.

In mid-July 2016, he underwent resection of the right lobe of the liver which contained a 1.5 x 4.0 x 2.7 cm well-circumscribed lesion. Microscopic examination showed “Metastatic nodule of colorectal-type adenocarcinoma with no residual viable tumor identified.” The finding of necrotic tissue, rather than viable cancer, is interesting since he had not received chemotherapy for more than a year.

He refused resection of the lung mass and continued on the protocol I prescribed, with no other treatment. A series of CTs have shown no further activity in the liver, and gradual shrinkage and disappearance of the lung mass. In March 2021, he told me that his oncologist marvels at the resolution of his Stage IV disease. Patient 1 has never told his oncologist about his nutritional program.

In summary, a liver metastasis developed in this patient while he was receiving FOLFOX chemotherapy. It was resected, and he began treatment with me roughly 10 weeks after surgery. Ten weeks later, scans demonstrated a recurrent liver lesion and a new lung lesion. The liver lesion was removed, and pathology showed “no residual viable tumor”; he had received no orthodox treatment of any kind during this window. Since then, the patient has had gradual resolution of the lung lesion, with no evidence for disease in several scans, while pursuing only the prescribed nutritional protocol.

In a review and meta-analysis of palliative chemotherapy for colon cancer, median survival was estimated to be 8.0 months for untreated patients and 11.7 months for the chemotherapy group.6 Patient 1 is now more than five years out from the discovery of metastatic disease.


Patient 2: Metastatic Non-Small Cell Lung Cancer

In October 2013, Patient 2 reported vision changes, vertigo, and headaches to his local doctor. Scans showed masses in his lung and brain, and in February 2014, the brain mass was resected. Pathology demonstrated “metastatic adenocarcinoma, most consistent with a non-small cell lung primary.”

March 2014 PET/CT revealed a 7 mm pulmonary nodule with intense uptake, and focal activity in the hilum. MRI of the head showed enhancement along the resection cavity. He then underwent radiation to the brain. 

He was told he would most likely be dead in six months regardless of treatment, so he refused chemotherapy and began a self-designed nutritional plan.  On this, his disease progressed. Chest CT August 2014 showed the lung lesion was larger at 1.5 cm, the hilar node also larger at 2.5 cm, and several new small nodules were seen, felt to be metastases.  MRI of the brain September 2014 showed a new 1 cm tumor in the frontal lobe; in a repeat scan in December, the frontal lobe mass measured 1.7 cm, and a new mass had developed in the cerebellum.

I first saw Patient 2 in late December 2014.  At that time, he felt well, though he did report visual changes caused by his original brain surgery.  He had no symptoms from his pulmonary disease.

In January 2015, he started the protocol I prescribed, but he also proceeded with glucocorticoids followed by radiation to both tumors in his brain, because of concerns about impending herniation.  After completing radiation, he developed excruciating headaches, and was found to have extensive vasogenic edema with midline shift.  In June 2015, he called to let me know that despite all these issues, he had stayed on the prescribed nutritional program.  Chest CT August 2015 showed that the previously seen masses had resolved. MRI of the brain September 2015 was unchanged from a June study. In March 2016, he let me know that a recent MRI of the brain demonstrated a slight decrease of enhancement in the resection bed, to the amazement of his neurologist.

During 2017 and 2018, he continued in his usual state of health, with visual problems felt due to his brain surgery and radiation. MRI of the brain April 2018, compared to a June 2016 scan, was read as “persistent right cerebral masses, slightly enlarged.” Then in late June 2018, he called me to report episodes of left-sided weakness and shaking. I told him to go the emergency room.

In the hospital, chest CT July 2018 showed “No evidence of metastatic disease or primary neoplasm involving the thorax.” An MRI of the brain, compared with the April 2018 study, showed “Interval increase in size of right frontal mass with signs of recent hemorrhage … with increased surrounding vasogenic edema … stable right parietotemporal mass with surrounding vasogenic edema.” His physicians concluded that the brain masses represented post-radiation changes, with the acute clinical change due to hemorrhage, and he was discharged on a glucocorticoid taper and levetiracetam.

I told him at the time that despite the clear chest CT, he should not assume that his cancer was gone, and should not stop his nutritional protocol. Unfortunately, because of his poor vision, and left-sided weakness from the June 2018 hemorrhage, he was never able to resume it. He lived alone, with very little social support, and was having great difficulty managing daily activities such as shopping, cooking, and cleaning. He contacted me occasionally to update me about his situation, and then again to let me know that his disease had recurred with a vengeance. He passed away in May 2020.

In summary, this patient with non-small cell lung cancer had one brain metastasis removed, then radiation to recurrent brain lesions, but had no systemic treatment and no treatment of any kind to the lung lesion or the hilar nodes.  While he was able to continue his nutritional program, there was no evidence of disease in the thorax; but after his neurological deterioration due to hemorrhage, he could no longer follow it; his disease recurred, and he expired.

In a review of cases of non-small cell lung cancer metastatic to the brain, median survival was about 10 months.7 Patient 2’s six-year survival is remarkable, as is the resolution of the lung tumor without orthodox therapy of any kind during the period he was able to follow his nutritional protocol. And while I am saddened by his death, in our last conversation he told me he was grateful for the extra time he had, and he promised he would put in a good word with St. Peter for me.


Discussion

The treatment protocol used with these patients involves three components: large doses of a pancreas product naturally rich in enzymes; diet and nutritional supplementation designed to address autonomic nervous system imbalance; and detoxification with several modalities, including coffee enemas. All three aspects are necessary for success.

Pancreas product. The theoretical mechanisms behind the use of pancreatic enzymes against cancer have been reviewed in detail elsewhere.8,9 To summarize, more than a century ago, the British embryologist John Beard noted the similarity between cancer and the trophoblast, the early stage of the placenta.10 Both tissues are undifferentiated, invasive, and able to create a blood supply. But at a certain point in gestation, the trophoblast modifies its aggressive behavior and transforms into the mature placenta. Beard observed that this transformation occurred at the same time the fetal pancreas began to synthesize enzymes, and speculated that pancreatic enzymes might play a role in cancer prevention and treatment.

Research has confirmed that trophoblast cells and cancer cells use similar mechanisms to invade and create a blood supply.11 More recent studies demonstrate receptors for proteases on the surfaces of both types of cells.12,13

During Beard’s life, physicians used enzyme preparations with variable success, which Beard felt was due to the erratic quality of the products used. Quality, dosing, and patient non-adherence all make for challenges in implementing this form of therapy. For some patients, it is difficult to accept that treatment will have to continue for years. Our belief is that cancer develops due to inadequate pancreatic enzyme manufacture by the body, and that just as an insulin-dependent diabetic requires insulin indefinitely, many of our patients require some additional pancreas product indefinitely or the cancer will recur. Patient 2’s story illustrates this.

Some patients over the years have decided that only the pancreas product is important and that they could minimize or eliminate the following aspects of the protocol. Kelley, Nick, and I all found that those patients do not succeed.


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