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The CAM therapies used by the patients are listed in table 4. Seventy patients stopped conventional medical therapy and chose to use only CAM. Within 2 months of therapy, 75% of these patients experienced recurrence or progression of disease, resulting in general ill health. Only 25% of patients experienced an improvement in general well being and body image, and had stable disease. However, all of the 200 patients who completed conventional medical therapy and used CAM either with the conventional therapy or afterwards had the benefit of mutual synergism of both modalities. These patients nurtured a hope for life and had better survival rates. The beliefs that led to patients choosing CAM were that this mode of therapy increases immunity, prolongs life, and cures cancer (table 5). It is clear that CAM alone does not help cancer patients to overcome this disease, especially when therapies are provided by unprofessional workers. Due to the lack of knowledge regarding the drugs given, in terms of efficacy and toxicity, patients¹ conditions often deteriorate to the extent whereby medical science can offer only palliative care. As a comparison, patients who continued with both treatment modalities experienced the benefits due to the synergism of both methods of therapy.
However, the exact mechanism of action is not known. In India, there have been no standardised treatment protocols or trials in favour of CAM therapy, although it is considered that ayurvedic and homeopathic medicine helps patients to some extent. All CAM needs methodical research, prospective trials, and proper categorisation before they can be advocated in daily clinical practice.
The first research work on CAM was initiated at the University of Texas MD Anderson Cancer Center (MDACC) and the School of Public Health in the USA. One of the first pilot studies conducted by the MDACC evaluated CAM approaches and assessed the impact of support groups versus imagery/relaxation practices on immune function, quality of life, and coping with treatment. Subsequently, the UT-CAM was established in 1995. The main aim of this centre was to evaluate the efficacy of biopharmacological and herbal therapies for cancer treatment, establish a CAM network for collaborative research, and improve self-assessment skills of CAM researchers. The first task of UT-CAM was to assess the state of the science and establish a research agenda. UT-CAM used multiple sources to identify agents, books, and consultations in the field.3 Subsequently, more than 30 therapies were identified for review and categorised as herbal, biological, pharmacological, or integrated regimens. This systematic review entailed an exhaustive search of libraries, databases, MEDLINE, Cancerlit, and Embase. The review yielded 6000 references of which 58.8% were related to cancer alone.
A survey conducted in 8 clinics at the MDACC assessed the use of CAM.4 Eighty three percent of 400 patients used CAM, of whom 62% used herbal tonics and vitamins. Overall, 64.5% did not discuss CAM with providers because they were uncertain of the benefit (54.0%) or because the physician did not ask (47.6%). The popular herbal tonic, Flora essence, was used extensively by cancer patients. The patients were asked about their agenda for seeking CAM. Surprisingly the beliefs were often overlapping, 53.2% reported that the tonic offered hope, 75.8% expected it to increase immune function, 59.2% believed it prolonged life, and 48.9% believed it cured cancer.
Herbal green tea extract, mainly mistletoe lectin III polyphenol, developed by liquid chromatography at the UT-CAM, primarily affects CD8 cells. The extract reduces the frequency of telomeric association and c-anaphases and reduces Bcl2 and p53 proteins.5 Water-soluble extract of oleander has a similar mode of action to polyphenol. Ginseng saponin is also used extensively throughout the world. Korean red ginseng saponins modulate carcinogenic metabolism and have an impact on precancerous lesions in rat colon. Compared with other herbal or biological agents, only ginseng significantly reduced aberrant crypt foci by 25% in the low dose group (0.1 gm/kg) but not in the high dose group (1 g/kg) [p < 0.05].6
Emodin, ellagic acid, resveratrol, and genistein purified from plants have optimum chemopreventive activity. In vitro studies of dolastatin 10 isolated from the molecule dolabella auricularia helps to prevent telomeric association, induction of polypoidy, and cell death. This molecule has a potent antineoplastic activity.7 Similarly, extracts from sea cucumber, phylum echinodermata, class holothurioidea, Q10 ubiquinone, melatonin, mistletoe, and shark cartilage are widely used by patients throughout the world, having an impact on analgesic consumption, weight loss, and tumour progression. However, no data on these agents are available.8 Preclinical pharmacokinetic testing and developmental phase I and II studies are necessary before starting clinical trials. Research should continue towards increasing knowledge of the importance of CAM for cancer therapy. Until then, patients hoping for survival will continue to believe in these therapies although there is currently no evidence base for these practices.
Regardless of their level of acceptance by conventional medicine, these therapies have infiltrated every aspect of health care. For many CAM therapies, data on characterisation of the product, standard protocols, reproducibility, safety, and basic pharmacology are lacking. We believe that CAM may help patients but more systematic research is needed to elucidate their methodology and acceptance. As indicated by the research activities of UT-CAM, preclinical, pharmacokinetic testing, and developmental phase I and II studies are necessary before these therapies can be integrated into clinical practice.
1. Ernst E, Cassileth BR. The prevalence of CAM in cancer. A systemic review. Cancer 1998;83:777-782.
2. Burnstein H, Gelber S, Guadagnoli E. Use of CAM by women with early stage breast cancer. J Am Med Assoc 1990;340:1773-1739.
3. Richardson MA, Postwhite J, Grimm E, et al. Coping, life, attitude and immune response to imagery and group support. Alternative Ther Health Med 1997;3:62-70.
4. Richardson MA, Ramirez T, Nanney K, et al. CAM implication for patient provider communication. Proc Am Soc Clin Oncol 1999; 18:590a.
5. Bussing A, Multani AS, Pathak S, et al. Induction of apoptosis by lectin on viscum album association with p53, Bcl-2 protein. Cancer Lett 1998;130:57-68.
6. Reuters Health Information. Federal panel focuses on CAM. Reuters Health 1999;July 12.
7. Stalker DF. Evidence and CAM. Mt Sinai J Med 1995;62:132-143.
8. Hoey J. The arrogance of science and pitfalls of hope. Can Med Assoc J 1998;159:803-804.
Address for correspondence:Dr R Kaul |