Antineoplastic Properties of Dietary Maharishi-4 [MAK-4] and Maharishi Amrit Kalash [MAK-5], Ayurvedic Food Supplements
European Journal of Pharmacology, Vol. 183, No. 2, p. 193, 1990 (Abstract).
H.M. Sharma,* J. Krieger,** and C. Dwivedi.**
**Department of Pathology, College of Medicine, The Ohio State University, Columbus, OH 43210
**College of Pharmacy, South Dakota State University, Brookings, SD 57007
Ayurveda (Ayu = life, Veda = knowledge, meaning the science of life) is an ancient medical science originated from Vedic tradition and widely practiced in India. Maharishi-4 (M-4) and Maharishi Amrit Kalash (MAK), ayurvedic food supplements belong to a group of substances known as rasayanas (Glazer, 1988). In ayurveda, rasayanas are given to bring homeostasis in the physiology, retard aging, and enhance vitality and immunity (Sharma, 1985).
M-4 and MAK have been shown to inhibit 7,12-dimethylbenz(a)antracene (DMBA)-induced mammary tumors in rats when given individually as a dietary supplement (Sharma et al., 1989). The purpose of this investigation is to study the effectiveness of the combination of M-4 and MAK dietary supplementation on DMBA-induced mammary tumors in rats.
Fifty-day-old Sprague-Dawley rats were divided into 4 groups, having 20 rats in each group. Group 1 (C) and group 3 (P) were placed on a rodent chow diet (Wayne Research Animal Diets, Chicago, IL, USA). Groups 2 (I) and 4 (I and P) were placed on rodent chow supplemented with 6% M-4 and 0.2% MAK (provided by Maharishi Ayurveda Products International). All rats were given DMBA (75 mg/kg in 1 ml of sesame oil) by gavage after being on the diet for one week. One week after DMBA administration, the I group was placed back on the normal diet and the P group was placed on M-4 and MAK-supplemented diets. Rats were weighed and examined weekly for the presence of mammary tumors for a period of 20 weeks. In the other set of the experiment, animals with mammary tumors were placed on either M-4 or MAK-supplemented diets. Tumor size was measured once a week for 4 weeks. Histopathologies of tumors from different groups were also performed.
After 20 weeks of DMBA administration, the tumor incidence was 60, 30, 25, 15% in C, I, P, and I and P groups respectively; the average number of tumor per rats was 0.65, 0.5, 0.35, and 0.35 for C, I, P, and I and P groups respectively. M-4 and MAK-supplemented diets caused tumor regression in 60% of rats. There was no significant difference in weight gain of rats in all the groups. The tumors from the C group had adenocarcinomas. The tumors from the I and P groups showed adenocarcinoma with extensive fibrosis and focal areas of necrosis and calcification. The tumors from the I and P group showed lobular adenofibroma with inflammation.
These results indicate the M-4 and MAK-supplemented diets protect against DMBA-induced carcinogenesis. Similar results were observed when M-4 and MAK were supplemented in the diet individually at the same dosages. The combination of M-4 and MAK together in the diet does not produce synergistic effects.
Abstract reprinted from European Journal of Pharmacology, Vol. 183, No. 2, p. 193, Copyright 1990, with permission from Elsevier Science.
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