（The Genetics of Scurvy and the Cancer Problem）
作者: Irwin Stone
对这种异常和危险的医学奇异现象负最大责任的是那些认为坏血病是他们的属地达60年的正统的营养学家，他们持续用一种不准确的假说盾牌、真假混杂和有问题的数据，攻击医学。他们以一个在1912年(Funk, 1912)创立的，在头20年提供了很大健康价值的理论开始。然而，他们没有认识到，所有理论都有其因为将来的研究结果而即将过时的规律性。过去10年关于抗坏血酸遗传学的研究提供了一个新的方法以认识它的病源学，以及为每天大量摄入抗坏血酸提供了一个更加理性的理论依据(Stone, 1966)。现在的指引是那些已超过他们的有效期的传统营养学观点，同时，对达致最佳的健康可能有潜在的危险。
过去10年的研究已经显示，现在公认的坏血病的疾病，实际上是称为“抗坏血酸缺乏症”（Hypoascorbemia）的潜在致命的肝酶疾病的终极后遗症。这种疾病是由于人类有一种有缺陷的，控制一种酶蛋白—L-古洛糖酸内酯氧化酶合成的基因，而引起的一种“先天性碳水化合物代谢错误”。在病源学上，它和许多其他遗传疾病如半乳糖血症，尿黑酸尿证，苯丙酮酸尿症和上千奇特的其他疾病相似。大多数其他的遗传疾病都是罕见的，但，抗坏血酸缺乏症令100%的人受累(Stone, 1966a)。将来对坏血病认真的研究应该在遗传范畴内进行，而不是由营养学家或家庭经济学家进行(Stone, 1967)。
早期研究抗坏血酸对癌症的治疗，回到1936年，在我的书“康复因子”（The Healing Factor）（出版于1972年），作了评述。这个研究显示，在CSS综合症和癌症之间，显示有实质性的联系。调查者的多数认为抗坏血酸为一种“微量营养素”，在一种精神压力如癌症这么严重的疾病，使用可怜的剂量，但尽管如此，他们仍可发现某种检测得到的临床成功。在这段时间内，没有任何经过周详策划和资助的实验，一次性测定抗坏血酸在这些疾病的实质性治疗潜力。
在1969年，国家癌症研究院(National Cancer Institute ,NCI)的BURK主任和他的研究小组在肿瘤杂志上发表了一份报告，描述他们的发现：抗坏血酸可以杀死癌细胞而同时，对正常细胞无害。句子开头这样写：“现在研究显示，在动物实验中（VITRO），抗坏血酸对Ehrich Ascites 癌细胞有高度毒性或致命毒性”。他们进一步写道：“抗坏血酸的显著优势。。。拥有作为潜在抗癌药，它们像青霉素，对正常身体组织，明显无毒，它们可用在动物上，在极大的剂量，（达到5或更多gm/kg）而没有可觉察到的有害药理作用。” 让我提醒你，对一个体重150磅的成年人，每公斤体重5克的抗坏血酸，等于350克或350,000毫克，超过3/4磅。
在1973年，出现了一篇由Ewan Cameron and Linus Pauling (Cameron and Pauling, 1973)发表的，关于用新的正分子方法治疗癌症和其他疾病的重要论文。这篇文章讲述了Cameron (Cameron, 1966)博士的最新研究结果。它显示，抗坏血酸是透明质酸酶的强力抑制剂。透明质酸酶是一种液化和穿破组织的酶而抗坏血酸可抑制它。所有细胞正常时都被包埋在抑制其生长的厚厚的粘液环境的基质中。细胞要生长和扩散，他们就释放可让细胞去分裂和扩散的透明质酸酶。只要有透明质酸酶释放，扩散就会持续，而不释放，扩散亦停止。而组织环境回到它正常的约束状态。也就说，抗坏血酸有减慢或制止癌细胞生长的潜力。让我从这篇文章引一些句子：“这个假说亦提示，在许多炎症和自身免疫疾病的一种安全和简单的控制方法。这些疾病，虽然具体原因仍然未知，但其基本的特征是，通常过度的细胞扩散。” “最重要的是，我们被引导至这样一个推论，这种无害的物质，抗坏血酸的使用，可能提供我们一种有效的方法，永久地抑制肿瘤细胞扩散和侵袭，也就是说，一种有效的控制癌症的方法。足够量的抗坏血酸可能是一种细胞生长繁殖抑制剂。” “我们希望，对这种安全物质进行一次深入彻底的实验，可能会得出，它是正分子医学的装备库里最有价值的物质。” “我们推论，抗坏血酸，可能有比分配给它的更大的治疗价值。”
第一篇(Cameron and Pauling, 1974)是抗坏血酸治疗癌症的理论依据的进一步讨论。第二篇(Cameron and Campbell, 1974)，报告一组50例晚期癌症病人，接受每日10,000毫克的抗坏血酸，口服或静脉注射，的临床实验结果。他们的推论是：“我们的临床发现支持这种基本主张，就是，大剂量的抗坏血酸提高对癌症的天然抵抗力。我们发现这种治疗，在处理末期“束手无策”的癌症中，有肯定的减轻价值。我们因此期望它，在治疗更早期的癌症和状况更好的病人，有甚至更大的价值。我们相信，不远的将来，大部分，如果不是在全部的癌症治疗方案，补充抗坏血酸将被承认作为一种标准的支持措施。我们认为，沿着这个方向的大规模的临床试验已被清晰地指明了。”
在卡车司机的病例，在重新开始抗坏血酸治疗时，其反应无白血病例的惊人。可能是由于这个事实，卡车司机比白血病病人得到更少的抗坏血酸。12,500毫克给予卡车司机，而白血病病人得到的是24,500~42,000毫克。12,500毫克的抗坏血酸，是一种处于治疗有效范围的下边缘的剂量。对一种如癌症如此严重和压力程度的疾病，每天口服至少50,000毫克的抗坏血酸将产生更有效的临床治疗反应。正如不仅被这种白血病例，同时亦被尚未发表的，William Saccoman 医生的临床数据所证实。
Cameron and Baird 在1973年(Cameron and Baird, 1973)，出版了重要的临床观察报告，就是，抗坏血酸的大剂量静脉注射，将缓解末期癌症病人的疼痛。五个需要定期以吗啡控制疼痛的病人，在10,000毫克抗坏血酸钠静脉注射的几天内，就可以完全中断吗啡的治疗。一个类似的止痛效果亦在许多年前被Klenner医生，在他用大剂量抗坏血酸治疗烧伤和毒蛇咬伤的时候注意到。当吗啡中断的时候，Cameron and Baird的病人没有任何戒断综合征出现。这可能提示，大剂量抗坏血酸在控制药物滥用问题是有用的。
最新出版的抗坏血酸的有效性的证据出现在1975年的11月的“外科”杂志上(De Cosse, 1975)，关于在消退直肠息肉中抗坏血酸的使用。每天给予，只需3,000毫克，缓释形式的抗坏血酸。尽管是这样低的量，作者说：“在8个病人的5个，抗坏血酸减少了直肠息肉的数量，并在其中3个显著减少了直肠息肉。” “我们把这个效果归功于抗坏血酸，这些效果提示，一些直肠肿瘤病变可能可以被药理方法逆转。”尽管用3,000毫克的临床结果几乎都是好的，有3个病人的直肠息肉未有对抗坏血酸治疗产生任何反应。这些无反应的病人将可能获益而且显示息肉减退,如果他们每天的抗坏血酸摄入量增加到我们现在所知道的产生惊人效果所必需的数量。在这种特别的情况下，在口服抗坏血酸的基础上，通过使用3%的抗坏血酸钠溶液灌肠，进一步的受益可能会出现。
Virginia Livingston 和 William J. Saccoman医生多年来都热衷于使用大剂量抗坏血酸治疗癌症。博Livingston医生，常规使用它作为其他用药程式的辅助，并取得很好的临床效果。Saccoman医生首先在末期癌症使用抗坏血酸。每天给予120,000毫克的抗坏血酸钠，作为一种灭菌、等渗的胃肠外的点滴溶液。他独立观察抗坏血酸钠的止痛特性。发现可以让病人去掉大量、有毒的吗啡定期注射。他获得了某些令人兴奋的指标，肿瘤在这些实验中消失。但不幸的是，他被迫突然、过早地中断了这项临床研究，过了一段时间，他才能重返和继续这项最有前途的癌症治疗。下列二例是已获得的典型结果。他的基本过程是，开始给予病人每天22,500毫克抗坏血酸钠，静脉注射，加上口服抗坏血酸和抗坏血酸钠，合共每天50,000毫克或直至腹泻为止。他发现腹泻在短时间内消失而维持病人在每天50,000毫克。静脉注射剂量逐渐减少，而同时，增加口服量，以维持这种每天的总量。最后，病人完全依靠口服，而病人的感觉是如此之好，以致可以在家里坚持这种不昂贵的治疗。这样大大减少了医疗护理开支。这种治疗的第一个注意得到的效果是病人“幸福感”的几乎立即改善。这二个病例说明，可以从这种无害的，非毒性的治疗得到什么？
我想提到另一个例子，一个离我家很近的人，这个项目的主席Bernard Rimland医生(Rimland, 1976)的女儿。经过六个月的不明诊断，她病得这样厉害，以致她的医生要把她立即送往医院住院治疗。1973年6月，因为严重的急性肾功能衰竭，她的肾脏镓扫描结果是这医院的医生历来看到最严重的。经过一个星期的检查，得出Hodgkin’s病的诊断结果，这个诊断在脾脏切除手术过程中再被证实和分期。这是最严重的阶段IV-B，这种病侵袭肾脏和肝脏。她的体重从患病前的103降到70磅。主治医生判断她的生存期少于一年。
The Genetics of Scurvy and the Cancer Problem
Irwin Stone 1
1 1331 Charmwood Square, San Jose, California 95117.
Transcript of a talk presented at the meeting of
The California Orthomolecular Medical Society, San Francisco,
14 February, 1976.
Scurvy is a very ancient disease and was known to the early Egyptians, Creeks, and Romans. Humans, from the time of their first appearance on this earth, have been constantly plagued by it. Being around for so long, there has been plenty of time to accumulate many misleading half-truths and misinformation about the etiology, incidence, pathology, and the dosages of ascorbate needed to control it. These misorientations have led to the present paradoxical situation where a large segment of the medical profession believes that scurvy is a very rare disease in this country, when actually nearly every patient who visits these doctors is also suffering from an insidious chronic form of scurvy in addition to the complaint that prompted the visit (Stone, 1972).
Before speaking about ascorbate and cancer, would like to take a brief historical look into how these half-truths and misorientations have lulled an uncritical Medicine into such a state of euphoria about scurvy that a large proportion of physicians are unable to discern the dangers to health in the present situation. This attitude has also been instrumental in retarding the full exploitation of the vast therapeutic potential of ascorbate since it first became available in unlimited quantities some 40 years ago.
Those most responsible for this unusual and hazardous medical paradox are the orthodox nutritionists, who have considered scurvy as their private domain for the past 60 years. They have continuously bombarded Medicine with a barrage of inaccurate hypotheses, half-truths, and questionable data. They started out with a theory in 1912 (Funk, 1912) that provided great health benefits in the first 20 years of its existence. However, they don’t realize that all theories have a built-in obsolescence, which is dependent on the results of future research. The research of the past decade on the genetics of scurvy provides a new approach to its etiology and a more sensible rationale for the quantitative daily intake of ascorbate (Stone, 1966). The present indications are that these traditional nutritional ideas have outlived their usefulness and may be potentially dangerous to full health.
The orthodox nutritionists regard scurvy as a simple dietary disturbance brought on by the lack of the micronutrient, vitamin C, in the foods consumed. Even the term, “vitamin C,” is a misnomer, so hereafter it will be referred to as “ascorbate.” Their interest in “micronutrients” has led them over the years to conduct very many tests on finding the “minimal daily requirements” for ascorbate to prevent the appearance of the classical symptoms of frank clinical scurvy, about 10 mg a day, but have not found a single long-term test conducted in the last 40 years for the purpose of determining the optimal daily intake of ascorbate to insure a lifetime of full health.
The research of the past decade has shown that the disease that is now recognized as “scurvy” is really the terminal sequelae of a potentially fatal genetic liver-enzyme disease called “hypoascorbemia.” This disease is an “inborn error of carbohydrate metabolism” due to humans carrying a defective gene for the synthesis of the enzyme protein, L-gulonolactone oxidase. It is similar in etiology to the many other genetic-enzyme diseases like PKU, galactosemia, alkaptonuria, and the thousand-odd others. Most of these other genetic conditions are of rather rare incidence, but hypoascorbemia afflicts 100 percent of the population (Stone, 1966a). Future serious research on scurvy should be within the province of medical genetics and not be conducted by nutritionists and home economists (Stone, 1967).
Probably the worst damage that has occurred resulted from their questionable data regarding the proper daily intakes of ascorbate. If you just want to avoid the terminal signs of the disease, then the vitamin-like levels are OK, but if you are interested in fully correcting this human genetic defect, then daily doses of ascorbate of a different order of magnitude are required.
Recent work has shown that during the course of the evolution of the vertebrates there has been an increasing demand and increased production of ascorbate within their bodies as they sequentially progressed from the amphibians through the reptiles, birds, and mammals. Ascorbate’s main functions during this evolution were as an antistressor, detoxicant, and to maintain biochemical homeostasis in the internal environment of the animal. A present-day mammal like a 150-pound goat is capable of making 13,300 mg of ascorbate a day (Chatterjee, 1973) to satisfy its daily needs for this metabolite and produces much more under stress. If humans had the intact gene, like most other mammals, it is nearly a certainty that they would be programmed to produce ascorbate in their livers at the same daily order of magnitude as these other mammals—thousands of milligrams a day. For the past 40 years the traditional nutritionists have regarded less than 100 mg a day of ascorbate as more than adequate for human needs.
Over the years they have had their Food and Nutrition Board of the National Academy of Sciences, the agency that sets the dietary standards and runs the nutrition show, consistently lower the Recommended Dietary Allowance, the RDA, for ascorbate. Their latest exploit in 1975 was to lower by 25 percent the already bare subsistence level of 1968. The adult RDA’s for ascorbate were 75 mg a day in 1958, in 1968 it went down to 60 mg, and now it is 45 mg (FNB-NAS, 1958, 1968, 1974). If they continue whittling away at this same rate in the future, the RDA will be zero by the year 2000!!
This present RDA of 45 mg a day may delay the appearance of the terminal symptoms of frank clinical scurvy, but it is very inadequate for fully correcting our inborn error of carbohydrate metabolism (Stone, 1974). This long-term poor correction of this genetic defect brings on the lifelong chronic subclinical scurvy, the CSS Syndrome, that develops in a population on these low intakes. It is my belief that this lifelong CSS Syndrome sets the stage for the present high incidence and morbidity of heart disease, cancer, the collagen diseases, kidney diseases, and the many infirmities found in the senior citizens. It is the only common thread that runs through all these diseases; all the victims of these diseases are also victims of the CSS Syndrome. Only when Medicine learns to correct this CSS Syndrome will we see the long overdue drop in the statistics of our serious medical problems.
Now let us see what the elimination of the CSS Syndrome can do in cancer.
The early work on the use of ascorbate in cancer, going back to 1936, was reviewed in my book, “The Healing Factor,” published in 1972 (Stone, 1972a). This work shows a definite link between correcting the CSS Syndrome and cancer. Many of the investigators thinking of ascorbate as a “micro-nutrient” used pitifully small doses in a disease as stressful as cancer, but in spite of this they were able to report some measure of clinical success. During this time there were no well-organized and well-financed tests to once-and-for-all determine ascorbate’s actual therapeutic potential in this disease.
Doses of 24,500 mg to 42,000 mg of ascorbate were first used in a case of myelogenous leukemia giving complete remission of the disease. This remission was due entirely to the ascorbate, because the doctor in charge of the case stopped the administered ascorbic acid, twice, as an experiment. Each time the patient’s temperature rose, he felt ill, and the leukemic symptoms returned. When the ascorbic acid was resumed, the temperature returned to normal within six hours, his malaise disappeared, and the remission reoccurred. This case history was published in the Medical Times 22 years ago (Greer, 1954), and you would think that someone in these many years would have tried this harmless megascorbic therapy in the thousands of cases of leukemia that appear each year. A search of the literature has failed to reveal anyone publishing a check on these exciting clinical results.
In 1969, Dean Burk and his group at the National Cancer Institute published in Oncology a paper describing their findings that ascorbate would kill cancer cells and was harmless to normal cells (Benade, 1969). The opening sentence reads, “The present study shows that ascorbate (vitamin C) is highly toxic or lethal to Ehrlich ascites carcinoma cells in vitro.” They wrote further, “The great advantage that ascorbates . . . possess as potential anticancer agents is that they are, like penicillin, remarkably nontoxic to normal body tissues, and they may be administered to animals in extremely large doses (up to 5 or more gm/kg) without notable harmful pharmacological effects.” Let me remind you that 5 g of ascorbate per kilogram of body weight, for a 150-pound adult, amounts to 350 g or 350,000 mg, over three-quarters of a pound.
They further state, “In our view, the future of effective cancer chemotherapy will not rest on the use of host-toxic compounds now so widely employed, but upon virtually host-nontoxic compounds that are lethal to cancer cells of which ascorbate . . . represents an excellent prototype.” They also point out that ascorbate was never tested for its anticancer effects by the Cancer Chemotherapy National Service Center, because it was too nontoxic to fit into their screening program. They don’t want to test anything unless it helps kill the cancer patient.
A substance like ascorbate that will kill cancer cells and be harmless to normal cells has been a long-term goal of cancer researchers, and in 1969 it looked like it had been achieved. One would expect that a crash research program would immediately be organized to check and extend these observations and obtain clinical data on this breakthrough. That was six years ago and no further papers could be found that were published by the NCI on this important subject. Apparently the work was stopped and dropped like a hot potato. If an intensive crash research program had been instituted in 1969, the cancer problem may have been solved by now, or at least we would know a lot more about the role of megascorbate in cancer.
In 1973 there appeared a very important paper on a new orthomolecular approach to cancer and other diseases by Ewan Cameron and Linus Pauling (Cameron and Pauling, 1973). This paper brought up to date earlier work by Dr. Cameron (Cameron, 1966) and showed that ascorbate was a good inhibitor of the enzyme, hyaluronidase. Hyaluronidase is the enzyme that liquefies and breaks down tissues and ascorbate prevents this. All cells are normally imbedded in a thick viscous environment of ground substance, which restrains growth. For cells to grow and proliferate, they release hyaluronidase, which permits the cells to divide, proliferate, and migrate. Proliferation continues as long as hyaluronidase is released and stops when it is inhibited and the tissue environment allowed to return to its normal restraining state. In other words, ascorbate has the potential of slowing down or stopping the growth of cancers. Let me quote a few sentences from this paper. “The hypothesis also indicates a safe and elegant method of control in many inflammatory and auto-immune diseases where, although the individual causes are still unknown, the essential feature is always excessive cell proliferation.” “Most important of all, we are led to the conclusion that the administration of this harmless substance, ascorbic acid, might provide us with an effective means of permanently suppressing neoplastic cellular proliferation and invasiveness, in other words an effective means of controlling cancer. Ascorbic acid in adequate doses might prove to be the ideal cytostatic agent.” “It is our hope that a thorough trial will be given this safe substance, ascorbic acid, which may turn out to be the most valuable of all substances in the armamentarium of orthomolecular medicine.” “We conclude that ascorbic acid may have much greater therapeutic value than has been generally assigned to it.”
Three further papers appeared in this series on this orthomolecular treatment of cancer, two in 1974 and one in 1975.
The first (Cameron and Pauling, 1974) was a further discussion of the rationale for the megascorbic therapy of cancer. The second (Cameron and Campbell, 1974) reported the clinical results of a pilot study of 50 advanced cancer patients receiving mostly 10,000 mg of ascorbate a day either intravenously or orally. Their conclusions were, “Our clinical findings support the general contention that large doses of ascorbic acid enhance natural resistance to cancer. We have found this medication to have definite palliative value in management of terminal ‘untreatable’ human cancer. We would therefore expect it to have even greater value when used in treatment of earlier and more favorable patients. We believe that, in time, ascorbic acid supplementation will come to be accepted as a standard supportive measure in most, if not all, forms of cancer treatment. We consider that large-scale clinical trials along such lines are now clearly indicated.”
The third paper (Cameron et al., 1975) is a case history of a “treatable” cancer in a 42-year-old long-haul truck driver. The diagnosis was malignant lymphoma and arrangements were started to have him treated by orthodox irradiation and cytoxic chemotherapy. Because of an administrative delay in sending him to the appropriate facility and his rapid clinical deterioration, ascorbate was administered in the hope that the malignant growth could be slowed until conventional treatment could be started. He was given 10,000 mg a day intravenously for the first 10 days and then 10,000 mg a day orally thereafter. The response to the I.V. ascorbate was so dramatic that the patient “claimed to feel quite fit and well and had been transformed from a ‘dying’ into a ‘recovering’ situation. Appetite had returned, night sweats had ceased, with a general sense of well-being.” The enlarged liver and spleen had receded and other symptoms of the disease rapidly subsided. The 10,000 mg of oral ascorbate was continued for five months and during this time he remained well and in active employment. At this time, for some unknown reason, the oral ascorbate was stopped. A month later at a routine clinical examination, he was sick and complained of a recurrence of the symptoms. Clinical evidence of return of the disease was obtained. Ascorbic acid at 10,000 mg a day orally was again given, but without the previous dramatic response. Two weeks later the disease had so progressed that he was readmitted to the hospital and given 20,000 mg a day of ascorbate, intravenously, for two weeks and then 12,500 mg a day orally thereafter. A slow and sustained clinical improvement was shown and examination about six months later showed him to be normal in all respects. “The patient remains fit and well, is in active heavy employment, continues to take ascorbic acid 12,500 mg a day and has no evidence of active disease.”
This case was described in detail because of the similarities of response to stopping the daily intake of ascorbate as in the case of myelogenous leukemia cited previously. In both patients the cancerous disease was in a state of remission during the large daily intakes of ascorbate and the disease returned as soon as the daily intake of ascorbate ceased. Control of the disease again occurred when the ascorbate was restarted.
In the truck driver’s case the response was not so dramatic on reinstituting the ascorbate as in the leukemia case. It is likely that this was due to the fact that the truck driver was getting much less ascorbate than the leukemic; 12,500 mg for the truck driver as against 24,500 to 42,000 mg a day in the leukemic.
12,500 mg of ascorbate a day is a dose that is in the lower fringes of therapeutic effectiveness for a disease that is so serious and stressful as cancer. Daily intakes of ascorbate of at least about 50,000 mg a day will give a more effective therapeutic response as indicated not only by this leukemia case but also by unpublished clinical data of Dr. William Saccoman, discussed later.
Doses of this order of magnitude can be given without fear of toxic responses. Dr. Klenner uses up to 300,000 mg of sodium ascorbate, intravenously, each day in his successful therapy of the viral diseases.
Cameron and Baird in 1973 (Cameron and Baird, 1973) published the important observation that intravenous megadoses of sodium ascorbate will relieve the pain in terminal cancer patients. Five patients on a heavy morphine schedule to control their pain were able to discontinue the morphine entirely within a few days after the 10,000 mg of sodium ascorbate injections were started. A similar pain-killing effect was noted many years ago by Dr. Kienner (Klenner, 1974) in his megascorbic therapy of severe burns and snakebite. No withdrawal symptoms occurred in Cameron and Baird’s patients when the morphine was stopped. This would suggest that megadoses of sodium ascorbate might be useful in the control of the drug abuse problem.
The most recent published evidence of the effectiveness of ascorbate appeared in the November, 1975, issue of Surgery (De Cosse, 1975) on the use of oral ascorbic acid in regressing rectal polyps. Only 3,000 mg of ascorbic acid, as a time-release preparation, were given each day. In spite of this low dosage the authors state, “Ascorbic acid reduced the number of rectal polyps in five of eight patients and caused a major reduction of polyps in three others.” “We attribute this effect to ascorbic acid. These results suggest that some neoplastic lesions of the colon may be reversible by pharmacological measures.” While their clinical results with 3,000 mg were mostly good, there were three patients whose polyps were unaffected by the treatment. These unresponding patients would probably benefit and show polyp regression if their daily ascorbate intake was increased to a level that we now know to be required for dramatic clinical effects. In this particular condition further benefits might occur through the use of 3 percent sodium ascorbate enemas in addition to the oral intake.
Both Dr. Virginia Livingston and Dr. William J. Saccoman of San Diego have been interested in the use of megadoses of ascorbate in cancer for many years. Dr. Livingston routinely uses it with very good clinical success as an adjunct to other cancer modalities. Dr. Saccoman first used ascorbate in terminal cancer, giving 120,000 mg of sodium ascorbate, as a sterile isotonic parenteral drip solution, a day. He independently observed ascorbate’s analgesic properties and was able to take these patients off their heavy, toxic morphine schedule. He obtained some very exciting indications that the tumors were dissolving in these tests, but unfortunately was forced to suddenly and prematurely discontinue this clinical work. It was some time before he was able to return and continue this most promising line of cancer therapy. The following two cases are typical of the results being obtained (Saccoman, 1975). His general procedure is to start the patients on 22,500 mg of ascorbate a day, intravenously, and an oral administration of ascorbic acid and sodium ascorbate to a total of 50,000 mg, or until diarrhea results. He finds the diarrhea clears in a short time and maintains the patients on a total of 50,000 mg of ascorbate daily. The I.V. administration is gradually reduced while at the same time increasing the oral intake to maintain this constant daily total. Eventually the patient is entirely on oral intake and is feeling so well as to be able to continue this inexpensive treatment at home and thus reducing substantially the cost of the medical care. The first noticeable effect of this treatment is an almost immediate improvement in the patient’s well-being. The two case histories indicate what can be expected of this harmless, nontoxic therapy.
1. An adult male had bladder cancer which metastasized to the spine at the level of the 10th thoracic vertebra. Surgical removal of this spinal cancer left the patient completely paraplegic. He was put on 50,000 mg of ascorbate and to quote the doctor, “he is now coming along beautifully.” There has been a return of bladder and bowel function and the patient is now able to walk with braces. The cancers are under control and dormant. During the day, the patient takes the powdered ascorbic acid and sodium ascorbate, and at bedtime takes eight of the time-release ascorbic acid tablets.
2. An adult woman was diagnosed as having carcinoma of the lung which had metastasized to the thoracic duct. This caused too much fluid to collect in the chest cavity as to interfere with breathing requiring 11 fluid drainages of the chest cavity. This cancerous invasion also caused giant ascites in the abdomen, so big as to cause an umbilical hernia, requiring surgical repair. Three years ago she was put on ascorbate, about 50,000 mg a day, and has been taking it ever since. The fluid in the lung and the ascites cleared and she has no signs of these any more. While the lung tumor is still present and visible in the x-rays, it is starting to calcify and there are no signs of active disease.
I would like to mention one other case, one that is close to home, the daughter of our Program Chairman, Dr. Bernard Rimland (Rimland, 1976). After about six months of undiagnosed malaise, she became so ill and weak that her physician had to immediately have her admitted to a hospital, in June of 1973, with severe acute renal failure. The gallium scan of her kidneys was the worst ever seen by the hospital staff. After a week of tests the diagnosis of Hodgkin’s disease was made, which was confirmed and graded during surgery for spleen removal. It was the most severe stage IV-B, with the disease invading the kidneys and liver. Her weight had gone down to 70 pounds from 103 pounds before the illness. The staff doctors gave her less than one year to live.
Shortly after the operation she was started on toxic chemotherapy. Each chemotherapy session made her extremely sick and totally incapacitated for 12 to 24 hours. She was also told that she would lose all her hair, which only further depressed her. On returning home from the hospital, Bernie put her on a high-ascorbate, high-vitamin and mineral regime, giving 30 g of ascorbate as a mixture of ascorbic acid and sodium ascorbate each day, orally. My time is running short so I can’t give you all the details of the beneficial results of this regime as reported by Bernie, but she did not lose her hair and a thorough examination six months after her surgery revealed that there were no signs of the active disease, and best of all she was feeling fine. Both the ascorbate and the toxic chemotherapy have been continued to the present, and she is now a very healthy young lady of 17, who is very active in school with a high scholastic average and a heavy schedule in dramatics and music that would fatigue any so-called “normal” high school student. There can be no doubt that the elimination of the CSS Syndrome in her case not only aided in survival but also speeded recovery and made normal living a reality. This illustrates the necessity for correcting the CSS Syndrome to counteract the toxic systemic effects of current cytotoxic therapy. Other cases of infantile leukemia successfully treated with ascorbate are known to Dr. Rimland, but I just don’t have enough time to discuss them.
If a physician has any doubts that the patients coming to them for help have this CSS Syndrome, this can be easily checked by means of a recently developed 10-second dip-stick urine test. It is called C-STIX and is available only from Ames Company in Elkhart, Indiana, and costs $6 for 50 plastic test strips. A C-STIX strip is dipped into a fresh sample of urine for 10 seconds, and the blue color developed by this immersion is compared against a series of blue color standards and the milligrams of ascorbate per 100 ml of urine is directly obtained. Sick people on bare subsistence intakes of ascorbate will either not spillover ascorbate into their urine or if they do it will be in the lower fringes of the test range.
The test is based on the observation made decades ago that if a “healthy” person is given 500 mg of ascorbate, he/ she will excrete about 50 percent of this test dose in a few hours. The observation was good, but it led to serious inaccurate conclusions. This high rate of excretion was assumed to mean that the body was fully “saturated” with ascorbate and that the “excess” was being eliminated. They did not know at the time that the percentage of excretion decreases with increasing test dosages. At 10,000 mg of ascorbate the spillover amounts to only about 20 percent, 8,000 mg remains in the body. So if you try this test don’t make this classic mistake. The test is suitable for detecting whether the patient is scorbutic and has the CSS Syndrome. It should not be used in its present form for determining optimal daily intakes of ascorbate. This should be done clinically.
The very simple lesson that Traditional Medicine must learn from the work reported here is that in cancer, as well as in other diseases, the victims are suffering from at least two diseases, of which one is the CSS Syndrome which can be so easily and harmlessly corrected. The full correction of this insidious syndrome by administration each day of the optimal intakes of ascorbate removes the present handicaps on the body’s recuperative and detoxifying powers and its normal ability to resist and fight off the disease and heal itself. No improvement in the present disheartening statistics on disease incidence and morbidity can be expected until this lesson is learned and practiced by the bulk of Medicine.
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CAMERON, E., and CAMPBELL, A.: The Orthomolecular Treatment of Cancer, II. Clinical Trial of High-Dose Ascorbic Acid Supplements in Advanced Human Cancer. Chem. -Biol. Interactions 9, 285-315, 1974.
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STONE, I.: Hypoascorbemia, the Genetic Disease Causing the Human Requirement for Exogenous Ascorbic Acid. Perspect. Biol. Med. 10, 133-134, 1966a.
STONE, I.: The Genetic Disease, Hypoascorbemia. A Fresh Approach to an Ancient Disease and Some of its Medical Implications. Acta Gen. Med. et GemeIl. 16, 52-62, 1967.
STONE, I.: Hypoascorbemia, Our Most Widespread Disease. Bull. Nat. Health. Fed. 18, No. 10; 6-9, 1972.
STONE, I.: The Healing Factor. “Vitamin C” against disease. Grosset and Dunlap Inc., New York, 1972a.
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From Orthomolecular Psychiatry, 1976, Volume 5, Number 3, pp. 183-190