Ovarian Cancer
In 2004, 25,580 women developed ovarian cancer in the United States, and 6,000 died from the disease, making it the leading cause of gynecological cancer deaths in women. (1) Ovarian cancer tends to occur in family clusters, with some 5% of all cases linked to inherited genetic aberrations, particularly mutations in the BRCA1 and BRCA 2 genes – mutations long associated with breast cancer as well. The protein products of two these alleles normally serve as tumor suppressors, so irregularities in the DNA encourage carcinogenic transformation.
The disease has also been linked to infertility, use of fertility enhancing drugs such as Clomid, and nulliparity. Each pregnancy reduces the risk, as does breast-feeding. Regular use of oral contraceptives actually lessens the risk of ovarian malignancy, while hormone replacement therapy doesn’t influence incidence either way, despite earlier concerns.
Ninety percent of women diagnosed with strictly localized disease survive five years, many of them cured by surgery alone. Once the disease spreads, ovarian cancer can be very aggressive, with fewer than 5% of stage IV patients living five years despite aggressive treatment. (2) Chemotherapy regimens that include one of the taxane derivatives, given along with platinum agents such as carboplatin, cut the recurrence rate for localized tumors and marginally improve survival for those patients with advanced disease.
As her symptoms worsened, AL, who knew of my work from a family member, decided to seek treatment with me for her neuromuscular problems. When she first came to my office in 1989, she had been off all medications for some three years, during which time her symptoms of weakness, nerve pain and numbness continued to progress. When I first saw her, she had no gynecological problems other than the history of a hysterectomy for uterine fibroids.
I designed a protocol to treat this patient’s muscle and neurological problems, without the high doses of enzymes we use against cancer. Subsequently, AL complied well with her program, and when I saw her for a return visit in August 1989, she reported her condition that had worsened without respite over the previous 10 years had improved significantly. She described a “20%” overall gain in motor strength and calf thickness, a marker her previous doctors had used to track her decline. The proximal muscle weakness in both legs had reversed to the point she could stand from a sitting position for the first time in years. However, on exam I detected a small pelvic mass and told her she needed to follow up with a gynecological evaluation upon returning home.
Some weeks later, in early fall, an ultrasound revealed a 7 x 8 cm cystic lesion posterior to the bladder. Then in early November 1989, at the Moffitt Cancer Center in Tampa, she underwent exploratory laparotomy and was found to have extensive malignant disease throughout her pelvis and abdomen. Her surgeon proceeded with bilateral oophorectomy, omentectomy, and extensive lymphadenectomy of pelvic, periaortic and precaval lymph nodes. The pathology report describes “Omentum diffusely infiltrated by papillary serous carcinoma” of ovarian origin, as well as tumor in both ovaries that involved both fallopian tubes. Cancer had infiltrated into all 21 of 21 nodes evaluated, and peritoneal washings were positive for “metastatic adenocarcinoma consistent with ovarian primary.”
After surgery, AL met with an oncologist who strongly recommended intensive chemotherapy, but she decided to refuse all conventional treatment, instead choosing to begin the cancer version of my therapy. At that point, I redesigned her regimen to include high doses of pancreatic enzymes throughout the day.
In December 1989 her oncologist wrote a summary note to me, which accompanied the records of her recent hospitalization. In his letter, he states:
She is diagnosed as having a Stage IIIC Grade I papillary serous cystadenocarcinoma of the ovary. I have recommended that she receive chemotherapy. She would be a candidate for GOG Protocol 104 intravenous Cisplatinum and Cyclophosphamide versus intraperitoneal Cisplatinum and Cyclophosphamide. Mrs.—- unfortunately did not wish to pursue the idea of chemotherapy.
She thereafter followed her program diligently for six years. By the mid 1990’s, her muscle weakness began to progress once again, making return trips to New York difficult, though she continued on the regimen and we worked together by phone. We last spoke in August of 1999, when she wrote after hearing me on the radio. She was 78 at the time, able to walk with a leg brace, and otherwise was doing fine, apparently cancer free nearly 10 years out from her diagnosis of extensive ovarian malignancy.
DeVita reports, regarding ovarian cancer patients such as this:
patients with stage III disease have a 5-year survival rate of approximately 15-20% that is dependent in large part on the volume of disease present in the upper abdomen. (2)
In this patient’s case, the disease did extend into the upper abdomen at the time of diagnosis. Furthermore, these survival statistics refer to patients treated with aggressive chemotherapy, which AL refused, choosing to follow only my regimen. Her prolonged disease free survival can only be attributed to her nutritional program.
In March 1993, during a period of extreme personal stress, the patient herself felt that the cysts had enlarged. An ultrasound at Johns Hopkins Hospital revealed:
…a large approximately 14 X 10 x 12 cm mass in the mid line pelvis… Multiple foci of hyper-echogenicity are noted… Therefore, this mass likely arises from the left ovary.
…Within the right ovary, there are two hypoechoic regions and a focus of calcification… The largest hypoechoic region measures approximately 1.5 x 1.6 x 1.5 cm.
At that point, her gynecologist insisted she undergo exploratory surgery, but JR instead returned to the Hippocrates Institute for a several week stay. Despite the aggressive dietary intervention, the mass continued to grow.
In mid-October 1993, JR returned to her gynecologist, with the large pelvic mass clearly evident. Another ultrasound revealed that the mass had grown considerably since March, now measuring “20 x 22 x 15 cm.” The radiology report states “This has moderately increased in size since the last examination… A normal right ovary is identified.”
JR then proceeded with surgery at Johns Hopkins Hospital after her physician agreed to remove only the mass and the associated ovary, not the uterus or right ovary. During the procedure, she was found to have a huge tumor that had penetrated into the recto-sigmoid area of the colon. Though the surgeon did preserve the uterus and right ovary, his resection was quite extensive as documented in the Discharge Summary:
The patient underwent surgery on November —1993, undergoing an exploratory laparotomy… resection of ureterosacral tumors, resection of left parametria, omentectomy, resection of rectosigmoid, left common iliac node dissection and para-aortic lymph node dissection
The pathology report describes an enormous tumor, “measuring 17 x 12 x 7 cm” consistent with “Adenocarcinoma probably serous,” though the tumor was finally classified as a clear cell subtype of ovarian adenocarcinoma. The lymph nodes appeared free of cancer, as did the right ovary. Since the disease appeared to be largely limited to the left ovarian mass, as big as it was and though the tumor had penetrated the colon, she was assumed to have “localized” stage I cancer.
Postoperatively, JR met with an oncologist at Johns Hopkins who strongly recommended chemotherapy. She initially agreed to the treatment, but after her discharge from Hopkins – with plans to return to start therapy – she then consulted with a second oncologist at George Washington University Medical Center, who was less insistent about the need for immediate treatment. JR therefore decided to refuse conventional approaches, though she did agree to return for routine surveillance. Note that a CA-125, a blood marker for ovarian cancer, was 16.1 at the time, within normal limits.
After learning of my therapy, she first came to my office in January 1994 and subsequently followed her nutritional therapy faithfully. When she returned for her first follow-up visit in April 1994, three months after she had begun treatment with me, she reported feeling “better than I have in years,” with significant improvement in her energy, stamina and well being. Shortly after that session, she experienced mild midcycle bleeding and consulted her local gynecologist, who felt a mass in the pelvis on exam. JR detailed the interaction with her oncologist in a note to me in late April:
I continue to feel great. What is so frustrating, though, is going to the doctor and being told something might be wrong when I am feeling the best I have in years. I think that on some level, Dr —-(the oncologist) hopes that something will be wrong so that he can prove to me that my program will not work.
Despite the concern, an ultrasound in May showed no lesions on the ovary, no fibroids, and a follow up exam with her gynecological oncologist was normal. Subsequent CA-125 tests all fell within the normal range.
JR continued doing well until mid-December 1995, nearly two years after she had started her nutritional program, when she developed sudden onset abdominal pain associated with nausea and vomiting. When the CA-125 came back elevated at 52 (normal less than 36), her oncologist immediately suggested radiographic studies. Before any testing could be done, her symptoms became so severe she went to the local emergency room, where an intestinal obstruction was ruled out. After intravenous hydration, she improved and went home, with a diagnosis of gastroenteritis. A repeat CA-125 in December came within the normal range at 22, and a CT scan showed a right ovarian cystic area, but nothing suspicious.
Since that time, JR has diligently followed her nutritional program, and is in excellent health. Her CA-125 has been within the normal range, the most recent level from 2005 coming in at 7. She excels at a stressful job that requires considerable travel, but nonetheless manages her nutritional program efficiently and effectively. Today, nearly 13 years after she began with me, she has no evidence of cancer, and has been able to avoid the intensive chemotherapy her doctors at Johns Hopkins aggressively pushed so long ago. Her long-term disease free survival to me is certainly intriguing.
In fact the two patients I have discussed with a history of ovarian cancer – AL and JR – both refused the chemotherapy that was strongly suggested after the initial surgery documented extensive disease. We find that patients with a diagnosis of ovarian cancer who have received, before consulting with us, multi-agent chemotherapy tend to have a more difficult course, with many ups and downs.
2. DeVita VT, Hellman S, Rosenberg SA. Cancer: Principles and practice of oncology, 6th Edition. Philadelphia: Lippincott Williams & Wilkins; 2001:1604.