Colon Cancer and Enzyme Therapy

In 2004,146,940 new cases of colon cancer were reported in the United States, and 56,730 deaths, making the disease the second leading cancer killer. (1) Only tumors of the lung claim more lives. The overall incidence has remained fairly steady over the past thirty years, while the mortality rate has dropped, perhaps due to public awareness campaigns emphasizing early diagnosis and regular colonoscopy in those over 50, the population most vulnerable to the disease.

Scientists over the years have proposed a number of causative factors, including inherited genetic abnormalities that may play a role in some 25% of all cases. Familial syndromes such as polyposis coli, in which afflicted family members can develop literally thousands of colonic polyps, significantly increase the risk for colon malignancies, as does inflammatory bowel disease, particularly ulcerative colitis. Colon cancer develops in up to 30% of patients with a history of colitis for more than 25 years.

Much if not most colon cancer has been linked to environmental factors, particularly diet. A number of studies support an association with a high intake of animal fat, presumably due to conversion of saturated fatty acids to carcinogenic compounds in the gut. A correlation between high serum cholesterol, obesity and colon cancer has also been proposed. However, recent studies suggest that fiber in the diet has little influence on incidence rates despite early positive reports claiming a protective effect.

Clinicians traditionally divide colon cancer into a four tiered “Dukes” staging system based on the depth of tumor penetration in the bowel wall and named after the researcher who in the 1930’s first proposed the schemata. In this hierarchy, Dukes A identifies cancer limited to the superficial layers of the colon with no invasion of underlying tissues. Dukes B indicates the tumor has invaded through the bowel wall but not into regional lymph nodes, Dukes C signifies the disease has spread into local lymph nodes, and Dukes D, the worst, means the disease has metastasized to distant organs such as the liver or lungs. Survival correlates directly with the Dukes’ stage at the time of diagnosis; more than 90% of patients with Dukes A live five years, while only 5%, if that many, of those classified as Dukes D last that long.

Studies going back 15 years confirm that chemotherapy with 5-fluorouracil and leucovorin administered after surgical resection of Dukes C tumors improves five- year survival by about 10% compared to those undergoing surgery alone. However, aggressive chemotherapy offers little long-term benefit once the disease has spread to distant sites.

Patient IL: A 4.5-Year Survivor

Patient IL is a 57-year-old man with a family history pertinent for a brain cancer in his mother, colon cancer in an uncle, and lung cancer in a second uncle.

He himself had generally been in very good health when beginning in 2000, he noticed a change in his bowel habits, including increased mucus in his stools, chronic indigestion, bloating and what he described as gas pains. He adopted a whole foods, vegetarian way of eating hoping for some relief, but over time his symptoms only worsened.

In mid 2001, he first noticed intermittent bright red blood in his stools. Some months later, in October 2001, he developed symptoms consistent with a bowel obstruction, including severe pain, bloating, abdominal distension, and an inability to move his bowels. When the symptoms resolved after several hours, he chose not to seek medical attention.

Several weeks later, in November 2001, the symptoms returned with a vengeance. He hoped once again to ride out the crisis, but over a three-day period the pain, bloating and distension worsened to the point he finally went to the local emergency room. A barium enema revealed an “apple core” lesion in the sigmoid colon indicating a tumor. When a subsequent sigmoidoscopy revealed a complete obstruction, the patient underwent emergency laparotomy, resection of the sigmoid colon along with the tumor, and placement of a temporary colostomy. The surgeon also discovered, as his operative note reports, “palpable nodules in the liver, which I felt to be more cystic than solid, but there were a couple studs that were solid.” He removed one of the liver lesions for evaluation.

The pathologist’s summary describes a large colon tumor, but doesn’t give exact dimensions, though it states “The mass locally grossly appears to extend to the underlying adipose tissue,” and defines the tumor as “moderately differentiated adenocarcinoma, extending through the bowel wall, and present on the serosal surface.” Though cancer had infiltrated two of nine lymph nodes examined, the liver tissue seemed most consistent with a benign hemangioma.

Postoperatively, a CEA test, a tumor marker for colon cancer, came back elevated at 5.1 (with normal less than 3), an indication of remaining malignant activity. No CEA had been done before surgery, so there were no results for comparison.

IL did subsequently meet with an oncologist who suspected the tumor had invaded the liver, despite the negative biopsy. He insisted chemotherapy needed to begin quickly, but upon questioning admitted if the cancer had indeed spread, treatment would do little. IL, who already had a strong interest in alternative medicine, decided to refuse conventional treatment and instead began self- medicating with a variety of nutritional supplements. After learning about our work from a local chiropractor, he chose to proceed with our treatment. He contacted our office in early January 2002, but we suggested he come in only after reversal of his colostomy.

Since the patient has been rushed into surgery in crisis from an obstruction, no preoperative CT scan had been done. Finally, in mid January, his doctors pushed for a scan, which revealed evidence of multiple metastatic lesions in the liver as the official report describes:

The radiologist also noted “very minimal subpleural densities seen at the mid left lung field” which he felt “should be rechecked within several months.” In his summary, he reports that “I suppose the liver findings increase suspicions of the left lower lobe findings however my feeling is that the lung changes will prove to be benign…”

Quite likely, based on the CT findings, cancer had spread into the liver and possibly to the lungs. The negative liver biopsy, the patient was told, might only indicate that the liver contained both benign and malignant nodules, as the CT scan seemed to show.

In late January 2002, the patient returned to surgery for reversal of the colostomy and lysis of adhesions that had formed since the first operation. During the procedure, unfortunately, none of the liver lesions were biopsied.

When IL was first seen in my office in mid March 2002, he seemed enthusiastic about the therapy and subsequently followed the regimen faithfully. Today, more than 4.5 years on treatment and five years from his original diagnosis, he remains fully compliant and enjoys excellent health.

Over the years that he has been my patient, IL has chosen not to undergo any further CT scans, a decision I have respected. He says no matter what the scans show, he wouldn’t agree to chemotherapy nor would he change his treatment. He doesn’t want the radiation exposure, which is significant, the worry, or the expense. So, I have no idea what has happened to the liver, or its lesions, I only know the patient is alive and well.

Even if we disregard the CT liver findings for a moment, a number of salient signs point toward a dismal prognosis. The literature reports that patients who initially present with an obstructing lesion have a far worse prognosis than those who don’t, even if the disease is otherwise localized. DeVita states in this regard:

Furthermore, in this patient’s case, the fact that the tumor had already invaded through the bowel wall and infiltrated into two lymph nodes signaled future trouble. The CEA level after surgery, though only mildly elevated, nonetheless also warned of a future recurrence – regardless of what may have been going on in the liver. Harrison’s reports that a high CEA before surgery, whatever the stage, suggests a poor prognosis:

IL’s elevated postoperative CEA served as an even more worrisome prognostic indicator. But finally, if we accept the expert radiologist’s conclusion that cancer had infiltrated the liver, the prognosis turns dire. DeVita reports median survivals in the range of 4.2 to 8.7 months for patients diagnosed with metastatic colon cancer receiving aggressive chemotherapy. (2) In a large-scale study. Manfredi et al report 1- and 5-year survival rates were 34.8% and 3.3% for synchronous liver metastases (meaning liver metastases occurring at the time of the original diagnosis of colon cancer). (4) These statistics include patients with solitary liver lesions, which can at times be resected along with the primary colon tumor, allowing for long term survival. In this case, IL, with multiple malignant appearing tumors on CT scan, not only has far outlived the predicted lifespan but has successfully avoided the toxic treatments his oncologist insisted five years ago needed to be done.

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1. Kasper DL, Braunwald E, Fauci AS, Hauser SL, Longo, DL, Jameson JL. Harrison’s Principles of Internal Medicine, 16th Edition. New York: McGraw-Hill; 2005:527.

2. DeVita VT, Hellman S, Rosenberg SA. Cancer: Principles and practice of oncology, 6th Edition. Philadelphia: Lippincott Williams & Wilkins; 2001:1227.

3. Kasper DL, Braunwald E, Fauci AS, Hauser SL, Longo, DL, Jameson JL. Harrison’s Principles of Internal Medicine, 16th Edition. New York: McGraw-Hill; 2005:530.

4. Manfredi S, Lepage C, Hatem C, Coatmeur O, Faivre J, Bouvier AM. Epidemiology and management of liver metastases from colorectal cancer. Ann Surg. 2006;244:254-9. [Abstract]