Melanoma originates in melanin synthesizing cells located in various pigmented areas of the body. Melanin gives color to the skin and provides protection against sun damage, and though we generally associate melanoma with the body surfaces, the disease can begin in the retina of the eye and even rarely, in the nasal sinuses.
Excessive sun exposure, especially a history of blistering sunburn in childhood, predisposes to the disease, particularly in those with light skin, red hair and blue eyes. A large number of moles also increases the risk, with 30% of melanomas developing in pre-existing nevi. Any change in a mole’s size, shape, or color (particularly to blue or purple), or bleeding from a nevus should alert the patient and physician to a possible problem.
Harrison’s states that in 2004, approximately 54,200 new cases were reported in the US, with 8,200 deaths. (1) Melanoma has attracted much attention in the research community because of its rapidly increasing incidence in the United States, with a 300% rise in the number of cases over the past 40 years. Scientists speculate that the dramatic change may correlate with increased recreational sun exposure, perhaps coupled with the shrinking of the ozone layer, which in times past may have more effectively reduced penetration of mutagenic ultraviolent light rays.
If diagnosed early melanoma can be cured with surgery in most cases. Once metastatic, the disease has a dismal prognosis, as Harrison’s reports:
Melanoma can metastasize to any organ, the brain being a particularly common site. Metastatic melanoma is generally incurable, with survival in patients with visceral metastases generally <1 year. Thus, the goal of treatment is usually palliative. (2)
Chemotherapy, immunotherapy and vaccine therapy have been heralded to some degree in recent years but none has proven effective to date once the disease has recurred and spread.
Patient VL, a research scientist, had been in good health when in the spring of 1983, he first developed persistent left sided sinus congestion. Over the next year, his doctors prescribed a variety of medications including steroids with little effect. An ENT physician diagnosed a deviated septum, so when his symptoms persisted, in September 1984 VL underwent surgery for septal repair. Incidental biopsy of a large nasal polyp revealed, unexpectedly, malignant melanoma of the sinuses. A CT scan after surgery documented a residual soft tissue mass in the right anterior ethmoid sinus, with destruction of the intrasinus wall.
The patient was then referred to Memorial Sloan-Kettering for further evaluation. In November 1984, at Memorial, VL returned to surgery for a left medial maxillectomy, with wide resection of the cribriform plate, resection of both ethmoids, frontal sinus, scraping of the mucosa of the sphenoid sinuses, and resection of the contents of the left maxillary antrum. The nasal septum and right superior turbinate were removed en bloc, and the floor of the anterior cranial fossa was reconstructed with a pericranial flap. The pathology report documents:
Residual malignant melanoma of the left ethmoid sinus mucosa with involvement of superior nasal septum. Tumor erodes underlying bone… All margins of resection are free of tumor residual disease, with apparently clean margins.
Postoperatively, the Memorial surgeon did not recommend radiation, which he felt would only cause tissue damage and interfere with healing of the reconstruction.
VL subsequently did well for a time. In late 1986 routine blood chemistries revealed an elevated LDH, a possible harbinger of recurrent cancer, but his local doctors pursued no additional investigations at that point. But in the late spring of 1987, VL developed persistent abdominal pain associated with bloating and indigestion. When his symptoms worsened, in July 1987 he returned to Memorial for a full metastatic work-up: a biopsy of the ethmoid sinus was negative for cancer, as was a CT scan of the head. However, an abdominal CT in July 1987 revealed a large abdominal mass, consistent with metastatic disease. In September 1987, he underwent exploratory laparotomy and was found to have massive adenopathy that collectively measured 12-14 cms in diameter positioned in the distal small bowel mesentery and invading several loops of small bowel. Tumor seeding was identified throughout the pelvis, and the large tumor mass had ruptured, forming a contained cavity adjacent to the terminal ileum. The surgeon resected the involved small bowel with primary anastomosis and debulked as much as cancer as possible, but much remained.
The pathology report describes:
Metastatic melanoma involving mucosa, submucosa and muscularis of a segment of small bowel. Melanoma also involves three mesenteric lymph nodes.
In a note to the patient’s local oncologist, the Memorial surgeon discussed the extensive abdominal cancer he had encountered, and his prediction of a poor prognosis:
As you know, a percutaneously guided aspiration revealed cells compatible with malignant melanoma, and at surgery, it was clear that the patients’ problem was due to massive adenopathy in the distal small bowel mesentery invading several adjacent loops of bowel and rupturing… The involved loops of bowel were resected with primary anastomosis, but the pelvis had seedlings of tumor adjacent to the major mass… For that reason and the fact that the tumor had ruptured and subsequently become contained by the adjacent mesentery, it was felt appropriate only to ‘debulk’ the mass… There is minimal gross disease left in the patient’s abdomen, but since seedlings had occurred and tumor had ruptured prior to surgery, the likelihood of diffuse melanomatosis is high…
While in hospital the patient was seen by Dr. —- who is in charge of our various melanoma research protocols including Interleukin-2, immunotherapy, etc. Dr —reviewed what is available at our Institution and the results of standard and experimental therapy here and elsewhere… I think he needs to digest what has been told to him, share it with his wife and discuss these options with his internists at home. He has a very poor prognosis, a tragedy in someone so young, courageous and knowledgeable. I only wish we had more concrete options to present to him. His training as a scientist allows him to understand our investigative protocols but also to realize that they are, indeed, investigation only…
With his options dismal, after recovering from his surgery VL began to consider alternative approaches. He learned of the late Dr. Robert Atkins, who in the late 1980’s sought to branch out from his diet work and began offering his own nutritional approach to diseases such as cancer (he eventually would abandon the effort to concentrate again on obesity).
In November 1987, VL began therapy at the Atkins’ Center in New York City. Initially, his disease seemed stabile, with a CT scan in January 1988 showing no overt evidence of recurrence. However, over the following months, VL developed an enlarging mass in his lower abdomen, visible on repeat CT scan in May 1988, and described as a “Recurrent 4.5 X 3.5 cm soft tissue mass in the region of the aortic bifurcation consistent with recurrent melanoma.” At that point, VL consulted with his Memorial surgeon who after reviewing the CT scan argued against further surgery which he said would be very debilitating and non-curative. He told VL that he might, if he were lucky, live six months.
VL had learned of my research study of Kelley, and heard I had recently begun seeing patients in New York. After discontinuing treatment with Dr. Atkins, he consulted with me in May 1988. On exam, he had obvious inguinal adenopathy as well as a hard, easily palpable large mid-pelvic mass. Thereafter, VL began his nutritional regimen, which he followed faithfully.
A baseline abdominal CT study in July 1988 – shortly after our first meeting – documented worsening disease since the prior scan. Not only had the mass grown slightly to 5 X 3.5 cm, but now the radiologist noted new adenopathy:
There has been a definite change since the study of 5/_/88 with left retroperitoneal and probably left lower mesenteric adenopathy now being present. Additionally, the mass described previously in the low left retroperitoneum has undergone slight further enlargement.
The tumors described in May and July were solid tumors, through and through, with no areas of necrosis. A follow-up CT scan in September 1988, when VL had completed four months on his regimen, showed slight increase in the size of the main tumor (4.5 x 6 cm.) but improvement in the adenopathy, as the official report states: “The previously described left periaortic adenopathy and mesenteric adenopathy is not as evident on this current study.” A CT scan three months later in December 1988 – six months after VL had begun his protocol – showed considerable improvement, with stabilization of the large mass and resolution of previously described adenopathy:
A lower left retroperitoneal prominent mass, described on earlier scan is again identified… it measures roughly 4.5 cm in AP diameter and roughly 5 cm. in width. This indicates little change in the size of this mass since the previous study. Left retroperitoneal adenopathy below the level of the renal hila, appreciated on the study of 7/_/88, is not clearly seen at this time… No mesenteric adenopathy is indicated on the current study.
During this time, VL felt well, in fact so well that he was able to resume his executive and scientific work full time. The next CT scan in June 1989 indicated:
Mass in the left periaortic retroperitoneal soft tissue is unchanged in size and appearance… mass unchanged since 12/22/88…
In late 1989, after he had completed some 19 months on treatment, VL wrote his surgeon at Memorial to inform him of his good health and apparent progress. The physician wrote back, saying:
Your letter of December — 1989 arrived during the Christmas season and carried with it much good cheer! I was thrilled to hear that your disease is stable and has bothered you no further since we last spoke in September of 1988… it is wonderful to know that you have done so well despite a rather frightening situation which we encountered during your operation in September of 1987…
In November 1990, VL’s internist ordered an MRI of the pelvis, which revealed that the previously solid mass had evolved into a more necrotic lesion: “This study is suspicious for a LEFT SIDED PELVIC MASS which may be necrotic…”
Over the next two years, VL remained extremely compliant with his nutritional therapy, enjoyed excellent health, and actually won an award for perfect attendance at his workplace. However, in the summer of 1992, after four years on his nutritional regimen, he became non-compliant with the prescribed diet, though he followed the supplement and detoxification protocols diligently. We have found over the years that for ultimate success, adherence to all aspects of the therapy absolutely essential. A patient who disregards the dietary recommendations is, in our experience, asking for trouble.
For our melanoma patients, we always prescribe a diet that emphasizes red meat, with the fat, preferably more than once a day. We forbid certain commonly enjoyed vegetables, such as leafy greens, and allow fruit only once a day, and never citrus. Such recommendations countered most expert recommendations emphasizing “low fat” and “no meat” that dominated the orthodox and alternative world during the 1990’s, particularly in regard to cancer. In this case, after VL’s daughter adopted a completely vegetarian way of eating, VL decided, without telling me, to switch himself to a similar diet in the summer of 1992, contrary to what I had prescribed.
By late fall 1992, his local oncologist felt, on physical exam, that the pelvic lesion had grown for the first time in years. An abdominal CT scan in December 1992 revealed a 7.0 cm soft tissue mass in the pelvis, containing areas of necrosis and calcification. The radiologist also noted a second 2.0 cm nodule, also showing areas of calcification, in the right abdomen at the umbilical level.
After a number of conversations with me, VL and I decided he should return to Memorial for surgery, since the mass was beginning to cause symptoms. His former physician, astonished VL was still alive nearly five years since his previous recurrence, agreed, after CT scans of the brain and chest were clear, to operate. In late January 1993 at Memorial, VL underwent “exploratory laparotomy, resection of tumor from mesentery/pelvis and right iliac vein and artery.” The tumors, the patient was later told, came out very easily, as if they had been encapsulated.
The pathology report from Memorial describes mostly dead tumor, with the main large main pelvic lesion described as “an 8 x 6 x 5.5 cm mass of predominently necrotic tumor tissue. The tumor is grossly present at the surgical margin.” The pathologist identified some residual viable cancer, described as “High grade malignant neoplasm consistent with metastatic malignant melanoma… Tumor is present at surgical margin.”
In an additional resected nodule, no viable cancer cells were found:
Mesenteric nodule excision: Necrotic tissue suggestive of a metastatic neoplasm largely replacing a fibrotic lymph node; cannot identify viable tumor cells.
A second node examined also appeared cancer-free. Overall, although some cancer remained, much of the original tumor evident in the spring of 1988 had died, now replaced by scar tissue.
According to the patient, while he was still recovering from the procedure, his surgeon met with him and discouraged him from consulting with any of the Memorial melanoma “experts.” He suggested that he only continue his nutritional program – advice given, VL said, “off the record.”
After recovering from his ordeal, and after several more lectures from me about the need for total compliance, VL resumed his full program – including the high red meat diet. He said he had learned his lesson. During the following eight years, he remained faithful to the treatment, enjoyed great health, retired from his job, and began a consulting firm. He also repeatedly expressed gratitude for the program, gratitude for the years of life the therapy had given him.
Unfortunately, beginning in 2001, after he had been on therapy for 13 years, I noticed a distinct change in attitude. He began to grouse about the program, about the “expense,” though money didn’t seem to be a problem for him, he complained about the supplement protocol, which required he take enzymes throughout the day. He repeatedly urged me to cut down the number of pills on his regimen, to make his life “easier.” I was reluctant to do so with his melanoma history, and in view of the fact that residual tumor remained after his 1993 surgery. Regardless of how well he had done, he was always at risk for recurrent disease. Eventually I relented, and reduced the number of enzyme capsules to what I considered a minimal dose. I later learned that VL decided without telling me to lower the dose still further, mistakenly thinking he was cured, that cancer could never be a problem again.
Despite the compliance lapses, VL did very well until late November 2003, when he developed chronic digestive problems, diminished appetite, and a seven pound weight loss. In mid-January 2004, he consulted his local physician who on exam detected new inguinal adenopathy. When I saw VL two days later in my office, in addition to the enlarged groin nodes I could now feel a new small mass in the mid abdomen. A CT scan the next day – his first scan in 12 years – showed:
INTERVAL DEVELOPMENT OF EXTENSIVE UPPER ABDOMINAL, PORTAL HEPATIS, AND SUPERIOR RETROPERITONEAL ADENOPATHY. MULTIPLE SPLENIC MASSES. SEVERAL TINY LOW DENSITY HEPATIC LESOINS ARE ALSO SEEN, NOT IDENTIFIED ON PREVIOUS EXAMINATION.
The disease had taken off. I immediately raised the dose of pancreas significantly, and VL agreed to do whatever he needed to do to fight back against the recurrent cancer. Unfortunately, his abdominal disease had progressed so far he had trouble eating, and in February both his local oncologist and I agreed surgical debulking might be helpful. VL called Memorial, only to learn his former surgeon – who had done the abdominal procedures in 1987 and 1993 – had retired. He consulted with the younger replacement, who felt the main abdominal mass was inoperable but strongly suggested he meet with a Memorial oncologist to discuss chemotherapy. VL, who well knew chemotherapy offered little benefit for his disease, declined the invitation. In early March, he did consult with an abdominal surgeon at Columbia, who concurred that surgery would not be feasible. But at Columbia the patient was aggressively encouraged to consider an interleukin II clinical trial, though the drug had proven to be a consistent failure for over a 15-year period.
VL did decide, despite my warnings, to consult with the interleukin II expert, who helped convince him to enter the study, to “shrink the tumors. In a later conversation with me, VL told me that feeling at the time somewhat desperate, he had agreed to proceed with interleukin just “temporarily,” to get him in better shape so he could follow my program more religiously. Ethically I could not tell him to refuse the treatment.
So in mid-March, VL went into the hospital for his first series of eight interleukin II treatments and during that time he could not follow my program at all. To my surprise, his doctors never expressed any interest in his 16-year survival with metastatic disease under my care, refused to speak to me about what they were doing, and when VL began to crash on the drugs, didn’t seem anxious even to talk with him.
After finishing the first course of treatment, VL went home to bed. After regaining some strength over a period of several weeks, he chose to re-enter the hospital for another round of interleukin. This time, the drug left VL far more debilitated, with severe anemia and weakness, and once home, he was unable to leave his bed for days. Not only was he exhausted and anorectic, but the bill for two weeks of treatment, he said, exceeded $200,000. By that point, VL decided to refuse all further conventional treatment, but he was so debilitated he could not resume my therapy.
A CT scan done in early May 2004 showed not only increase in the size of the previously noted tumors despite interleukin, but new lesions in the liver as well. The treatment had done nothing but make the situation worse. A local oncologist suggested chemotherapy; his friends began suggesting a variety of odd treatments including a special immunotherapy available only in Argentina. I urged him to rest, to regain his strength, and try to restart his nutritional program, which had beaten back his disease in the past. Instead, VL flew to California to consult with a well known melanoma expert and surgeon at the John Wayne Cancer Center, hoping this physician might be able to resect the tumor. But after several meetings, VL was told surgery would not be possible.
VL returned home, only further tired from the trip. He remained anemic, exhausted, debilitated. He was angry he had ever allowed himself to be talked into the course of interleukin. In mid June, we had a long conversation about the situation, reported in my office notes:
He is very upset about the interleukin experience… He said he wrote to Dr. —but never heard a word. No one has followed up. He said it is as if they do not care after spending a couple hundred thousand dollars on two sessions… They just do not care he feels.
A week later, not having resumed his nutritional treatment, VL finally died at age 73,16 years after he had begun treatment with me in 1988, when his predicted life expectancy was only months. Certainly, his long survival is extraordinary, as is his significant reduction of disease during his first years on therapy when he followed his prescribed regimen diligently. In the fall of 1992, when he decided to adopt a diet completely unsuited for his metabolism (by our standards) his disease progressed. When his compliance improved after surgical debulking, he remained disease free for 11 years, despite the aggressive nature of his cancer. After his compliance flagged, he ultimately suffered an explosive recurrence in early 2004, and was unable to resume his full program. Well meaning friends, his own fears, and the power of orthodoxy ultimately led him to an ineffective course of interleukin that left him considerably weakened and with his disease worsened. Nonetheless, though he ultimately died, he had many productive and very happy years. We do miss him.
Patient QM is a 72-year old man who had been in excellent health when in July 1990 a pre-existing mole on his left ear suddenly enlarged and turned black. When the lesion continued to grow, in January 1991 QM went to his local physician who immediately referred him to a surgeon. He then underwent excision of the lesion, which proved to be melanoma, Clark’s level IV, with a 1.9 mm depth.
In late January 1991 QM returned to surgery for a neck dissection, superficial parotidectomy and excision of the left ear in toto. The pathology report describes residual melanoma in the original site to a depth of 1.2 mm, but the lymph nodes and parotid were free of cancer. His doctors warned the disease might recur, but recommended no additional treatment.
In June of 1991, just five months after his major surgery, QM developed two nodules in the left mastoid area adjacent to the previous surgical incision, as well as a nodule in the skin of the right axilla. In late June, he consulted his surgeon, who removed the lesions:
… at a recent follow up visit in June I noted that he had a couple of little nodules under the skin of the mastoid area on the left adjacent to the ear resection and he also showed me another little clump of nodules in and under the skin of the right upper arm. I excised all these under local anaesthetic and histology of that has confirmed that all three are malignant melanoma…
I have put QM and his wife fully in the picture about the fact that his melanoma appears to have spread by the bloodstream and may turn up at other distant sites in the future.
After the surgery, QM underwent a full metastatic work-up. A chest x-ray was clear, as were CT scans of the head, head, chest and abdomen. However, QM’s doctors advised him that his disease would recur and prove terminal, most likely within a year. No further treatment with either chemotherapy or radiation was thought warranted, due to its ineffectiveness.
QM began investigating alternatives, learned of my work and first came to my office in September 1991. At that time, he felt well and had a normal physical examination except for evidence of his extensive head and neck surgery. He thereafter proved to be a very compliant patient, and on treatment, he felt well and continued his demanding career. When seen in March 1993, after completing 18 months on his nutritional regimen, he felt fatigued from overwork and frequent air travel, but otherwise appeared well.
When I saw him 19 months later, in October 1994, after three years on the regimen, he reported increasing stiffness in his neck and symptoms consistent with optical migraines occurring 1-2 times a month. When his headaches worsened upon returning home, he consulted with a neurosurgeon. A CT scan of the brain revealed a 4.5 x 2 x 2 cm mass in the right occipital area of the brain. Since the tumor appeared easily accessible, the surgeon strongly recommended resection, and after discussing the situation by phone with me, I agreed he should proceed with surgery, the sooner the better. So, in mid December 1994, QM underwent craniotomy and excision for what proved to be an encapsulated melanoma tumor. The pathology report states:
Sections show a discrete tumor mass bounded by gliotic brain. Tumor extends to margin of excision in some sites. There are conspicuous lymphocytic collections around the tumor. The tumor consists of sheets of poorly differentiated cells. A few contain granules of melanin. There are areas of necrosis.
He had no further conventional treatment, and resumed his program as soon as he returned home from the hospital. Initially, he felt quite well, with his neurological symptoms resolved but by February 1995, just two months later, he once again developed persistent headaches. A CT scan and MRI of the brain confirmed that a tumor had regrown in exactly the same location as the prior lesion. His surgeon felt that once again the tumor could be easily resected, so after multiple phone consultations with me, in early March 1995 he underwent repeat craniotomy and excision of the mass. The pathology confirmed “recurrent metastatic amelanotic melanoma.” The report elaborates:
The appearance resemble those of the previous biopsy, but now inflammation is less obvious and there is much more necrosis.
His local doctors suggested two doses of localized stereotactic radiation, to eliminate any lurking malignant cells in the tumor bed, and I concurred with the recommended treatment. QM tolerated the radiation well, and subsequently continued on his nutritional program, which I adjusted to take into account the recent series of events. After that, he experienced no further recurrence, and today, nearly 12 years from his last surgery, he remains compliant with his full regimen, now 15 years since he first consulted with me. He is in excellent health, and continues his productive professional life.
As I put this case together, although a CT scan of the brain in July 1991 showed no tumor, he didn’t start his nutritional program until early October, a full three months later. Given the nature of his disease and its tendency to spread and kill quickly, it is possible the brain lesion first grew in the interim before he started treatment with me. During that three-month period, he was on no therapy whatsoever, and it is also possible that once he began treatment, tumor growth slowed. In my experience, it would be unusual to see, in a fully compliant patient, new tumor forming.
In late 1994, QM traveled considerably, and perhaps this physical stress, not an inconsequential variable, weakened him enough to allow the tumor to grow despite his good compliance. But then, within two months of the first brain surgery, the tumor recurred in the same exact location. We do find that in areas of prior surgery, blood circulation, and with it the enzyme supply, can be compromised due to fibrosis and scar formation. In such protected areas, sometimes tumors can reform, though rarely do they spread beyond the scarified boundaries. The fact that in the nearly 12 years since his second surgery QM has remained completely cancer free indicates something unusual was going on in that particular area of the brain in 1994. I admit what I propose above falls into the realm of conjecture, but it’s important to keep in mind that metastatic melanoma usually kills within months, regardless of the conventional therapy, such as radiation, that might be employed.
Metastatic melanoma has a median survival of only 6 to 9 months and current systemic therapy has been shown to induce complete durable responses in only a small minority of patients. (3)
The DeVita chapter on melanoma has a section devoted to brain metastases specifically. In this case, the author writes of the dismal prognosis even when the disease is treated aggressively:
A series of patients with symptomatic solitary intracranial lesions showed a median survival after craniotomy of only 10 months.
Radiation offers little additional survival benefit to surgery.
Finally, I want to remark about this patient’s attitude toward me, and the program. When he developed evidence of recurrence in December 1994, he didn’t immediately assume the program had “failed,” and that I didn’t know what I was doing. Quite the contrary, he understood he had terrible disease, and he knew his survival even at that time was unusual. Though perplexed by the recurrence, he listened carefully to my hypothesis that perhaps this tumor was not new. When the disease recurred two months later, he again assumed that the therapy would eventually gain control of the situation, as it apparently has over the past 12 years. At no point did ever lose faith in the treatment, or in me, and within days of each of his two brain surgeries, resumed his full program with only greater devotion.
Patient IJ is a 68-year-old man with a history of significant sun exposure when younger, including summer stints as a lifeguard. He first developed skin cancer in 1987, thought secondary to excessive sun damage. Over the following year, his dermatologist removed 12 basal and squamous cell carcinomas from his chest, back and face. Then during a routine follow-up exam in 1988, IJ was found to have a suspicious lesion in his scalp above his left ear. This was removed in September 1988, and described as “malignant melanoma, near left ear, measuring at least 1.3 mm in greatest thickness.” A chest CT at the time showed no evidence of metastatic disease.
Shortly after surgery, in the fall of 1988, IJ detected a new lesion anterior to his left ear. Initially, his surgeon and dermatologist were unconcerned, but when the lesion continued to grow, he was admitted for evaluation to a New York City hospital in August 1989. After CT scan studies of the brain, chest and abdomen were negative for metastasis, IJ underwent left superficial parotidectomy and left radical neck dissection. The pathology report describes “Metastatic malignant melanoma to intraparotid gland lymph node,” but no other areas appeared infiltrated with cancer.
However, a postoperative CT of the neck showed a new subcutaneous lesion in the back of his head, in the occipital area. At this point, IJ, aware of his dismal prognosis with recurrent melanoma, began investigating alternative approaches to cancer, learned of our work, and first consulted with me in November 1989. During my initial examination, I detected a small 0.5 cm nodule in the scalp of the right occipital area, as well as many areas of sun damage on his chest and back.
Subsequently, IJ proved to be a very determined, compliant patient. By March of 1990, when he came to the office for a routine visit, the occipital lesion had completely regressed. Thereafter, as he continued his program diligently, he reported an overall improvement in his general health and returned to work after a medical leave to resume leadership of a successful business.
Over the next two years, his dermatologist removed several small pre-existing superficial basal and squamous cell carcinomas in sun-damaged areas, but his melanoma did not recur. After 1992, he developed no more skin cancers while following with his nutritional regimen.
IJ continued on therapy fully for some five plus years, before his compliance fell off during mid 1994. In July 1996, after an 18-month absence, he returned to the office and reported he had adhered to the prescribed diet and continued the detox procedures including the coffee enemas, but had gradually dropped off the supplement protocol. He felt “great” and admitted he had gotten careless since his diagnosis of recurrent melanoma seemed so far in the past. After that visit, I periodically heard from him by phone but I didn’t see him in the office again until May 2001. He told me that after following the full regimen for a another year or two after the 1996 visit, he had gradually drifted away from the supplements once again. In early 2001, he had developed a nodule on his left shoulder, which had been excised in March 2001 and found to be not melanoma, but a cutaneous leiomyosarcoma. After experts at the Armed Forces Institute of Pathology confirmed the diagnosis, IJ had undergone a wide excision of the original area, but no additional cancer was detected.
He also reported that after stopping the supplements, he had once again developed a number of squamous cell carcinomas of the skin after being cancer free for years. But after our May 2001 visit, IJ resumed his full nutritional program, which he followed faithfully for more than a year, before again slacking off the supplement regimen. However, neither his melanoma nor his sarcoma have recurred; he recently reported to my office staff that he was in “great shape,” cancer free since his last bout in 2001.
Clearly, this patient’s course has been unusual. He had a history of poor prognosis, recurrent melanoma, with, at the time he first consulted me, evidence of a suspicious new lesion in his skull. This nodule regressed quickly and completely on our therapy. During his first two years on the regimen, a number of basal and squamous cell carcinomas were removed, but these I suspect had been festering for years. Eventually, as long as he followed his program fully, no new malignant skin lesions developed.
IJ ran into trouble after his compliance fell off in the late 1990’s, when once again squamous cell cancers, but no melanoma lesions, began forming. After he developed cutaneous leiomyosarcoma in 2001, he resumed his protocol and remains today, 17 years from our first meeting, cancer free.
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; 2005:496.
2. Kasper DL, Braunwald E, Fauci AS, Hauser SL, Longo, DL, Jameson JL. Harrison’s Principles of Internal Medicine, 16th Edition. New York: McGraw-Hill; 2005:503.
3. DeVita VT, Hellman S, Rosenberg SA. Cancer: Principles and practice of oncology, 6th Edition. Philadelphia: Lippincott Williams & Wilkins; 2001:2048-50.