Are any of the Major Disease's Treatable or Curable with Holistic Therapies?
According to a Los Angeles Times report,“Over 75 per cent of the oncologists polled said that if they had cancer, they would never use the same chemotherapy they prescribe for their patients, because of the ineffectiveness of chemotherapy, and its unacceptable degree of toxicity.”
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Chemotherapy and radiation kill cancer cells, but harm the immune system. The temporarily suppressed cancer often reappears, since the body cannot defend itself with weakened immunity. “How much better it is to nourish the immune system directly by the use of natural therapies to assist it in getting you well, instead of destroying it by the use of these therapies! Then the immune system itself can kill the cancer cells without any side-effects, and heal your body at the same time,” writes Dr Loraine Day, M.D., who cured her breast cancer naturally.
Modern oncology (study of tumours) is based on the Halstead theory by W S Halstead. He focussed on treating and removing tumours to cure cancer. But cancer mortality rate remains unchanged despite advanced surgical techniques and aggressive modern treatments. Halstead’s theory is inadequate because it ignores the patient as a whole living organism.
“While conventional medicine primarily treats cancer as a focal disease with localized symptoms, naturally oriented physicians…view the body as a closed internal ecosystem, and believe that the dysfunction of this ecosystem leads to the development of cancer,” writes Dr Michael Lam, a top US-based physician and author of the book, Beating Cancer With Natural Medicine.
Deepak Chopra, the apostle of Ayurveda and mind/body medicine, in his book, Quantum Healing, asks, “Why, when your body mends a broken arm, is it not considered a miracle, but when your body rids itself of cancer, it is?” Blending advanced physics with ancient Indian Ayurvedic insights, he shows that the human body is governed by a ‘network of intelligence’ grounded in quantum reality. This intelligence exists in our 50 trillion cells, and a cell can heal itself of even cancer. Strengthening of immunity, healthy lifestyle, diet, exercise and access to the Divine consciousness within, through yogic and meditative disciplines, can correct the wrong information that triggers uncontrollable cell multiplication, and cure cancer from the quantum level of the body.
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Fucoidan cures infection with both antimony-susceptible and -resistant strains of Leishmania donovani through Th1 response and macrophage-derived oxidants.
Molecular Cell Biology Laboratory, Infectious Diseases and Immunology Division, Indian Institute of Chemical Biology, Kolkata, India.
Abstract
Objectives The aim of this study was to evaluate and characterize the antileishmanial efficacy of fucoidan, a polyanionic sulphated polysaccharide from brown algae, in experimental infections of BALB/c mice with antimony-susceptible (AG83) and -resistant (GE18ER) Leishmania donovani. Methods The effect of fucoidan was assessed against intracellular parasites in cultured macrophages and in suppressing splenic and liver parasite burdens in a BALB/c mouse model of visceral leishmaniasis by microscopic evaluation of surviving intracellular amastigotes stained with Giemsa. To evaluate the type of immunological responses, real-time PCR and ELISA were performed for various Th1 and Th2 cytokines in both in vitro and in vivo infected conditions. To determine the effector mechanism, reactive oxygen species (ROS) and NO were measured in fucoidan-treated animals by H(2)DCFDA-based fluorometric analysis and Griess reaction, respectively. Results In addition to having appreciable inhibitory effect on amastigote multiplication within macrophages (>93% inhibition at 50 μg/mL), complete elimination of liver and spleen parasite burden was achieved by fucoidan at a dose of 200 mg/kg/day given orally, 3 times weekly, in a 6-week mouse model of both antimony-susceptible and -resistant strains. This curative effect is associated with switching of T cell differentiation from Th2 to Th1 mode. Further, splenocytes of fucoidan-treated infected (AG83 and GE18FR) mice generated significantly enhanced levels of superoxide and NO. Not only was this treatment curative when administered orally 15 days post-infection, but it also imparted resistance to reinfection. Conclusions These results suggest the effectiveness of fucoidan as potent immunomodulator for controlling both antimony-susceptible and -resistant visceral leishmaniasis.
Fucoidan from Undaria pinnatifida Induces Apoptosis in A549 Human Lung Carcinoma Cells.
Department of Molecular Medical Science, Institute of Medical Science, St Marianna University School of Medicine, Kawasaki, Japan.
Abstract
BACKGROUND: Human T-lymphotropic virus type-1 (HTLV-1) is a human retrovirus that causes HTLV-1-associated myelopathy/tropical spastic paraparesis (HAM/TSP) and adult T-cell leukaemia (ATL). A higher viral load in individuals with HTLV-1 infection increases their risk of developing HAM/TSP and ATL. Moreover, the high proviral load is associated with the clinical progression of HAM/TSP. Reduction of the number of HTLV-1-infected cells is therefore crucial for preventing and treating HTLV-1-associated diseases. Recently, fucoidan, a complex sulphated polysaccharide derived from marine seaweed, has been demonstrated to exert inhibitory effects on HTLV-1 infection in vitro. In this study, we examined the in vivo effects of fucoidan on HTLV-1 infection.
METHODS: In this single-centre open-label trial, 13 patients with HAM/TSP were treated with 6 g fucoidan daily for 6-13 months. The HTLV-1 proviral DNA load and frequencies of HTLV-1-specific CD8(+) T-cells, natural killer cells, invariant natural killer T-cells and dendritic cells in the peripheral blood were analysed. Furthermore, the in vitro inhibitory effect of fucoidan on cell-to-cell HTLV-1 infection was examined by using luciferase reporter cell assays.
RESULTS: Fucoidan inhibited the cell-to-cell transmission of HTLV-1 in vitro. Furthermore, fucoidan therapy resulted in a 42.4% decrease in the HTLV-1 proviral load without affecting the host immune cells. During the treatment, no exacerbation was observed. Four patients with HAM/TSP developed diarrhoea, which improved immediately after stopping fucoidan administration.
CONCLUSIONS: Fucoidan is a new potential therapeutic agent for the prevention and treatment of HTLV-1-associated diseases.
Fucoidans from Brown Seaweeds Sargassum hornery, Eclonia cava, Costaria costata: Structural Characteristics and Anticancer Activity.
Pacific Institute of Bioorganic Chemistry of Far Eastern Branch of the Russian Academy of Sciences, Vladivostok, 690022, Russia, svetlana_ermakova@hotmail.com.
Abstract
Fucoidans were isolated by water extraction and ion-exchange chromatography from brown algae Eclonia cava, Sargassum hornery, and Costaria costata collected near of Korean coasts. The structures of fucoidans were investigated. Fucoidan from E. cava was mixture of sulfated rhamnogalactofucan and galactofucan. Fucoidan from C. costata was a sulfated galactofucan. Fucoidan isolated from S. hornery was separated into three fractions: a homofucan sulfate, a homofucan but without sulfate groups, and a sulfated rhamnofucan. The results clearly showed that fucoidans play an inhibitory role in colony formation in human melanoma and colon cancer cells and may be effective antitumor agents.
Relationship between oversulfation and conformation of low and high molecular weight fucoidans and evaluation of their in vitro anticancer activity.
Department of Marine Food Science and Technology, Gangneung-Wonju National University, Gangneung, Gangwon 210702, Korea. bylee@cha.ac.kr
Abstract
Low and high molecular weight fucoidans (F(5-30K) and F(>30K)) were chemically modified through the addition of sulfate groups, and the effect of oversulfation on the in vitro anticancer activity was investigated. After the addition of sulfate groups, a considerable increase of 35.5 to 56.8% was observed in the sulfate content of the F(5-30K) fraction, while the sulfate content of the F(>30K) fraction increased to a lesser extent (from 31.7 to 41.2%). Significant differences in anticancer activity were observed between the oversulfated F(5-30K) and F(>30K) fractions, with activities of 37.3-68.0% and 20.6-35.8%, respectively. This variation in the anticancer activity of oversulfated fucoidan derivatives was likely due to differences in their sulfate content. The results suggest that the molecular conformation of these molecules is closely related to the extent of sulfation in the fucan backbones and that the sulfates are preferably substituted when the fucoidan polymers are in a loose molecular conformation.
Received April 26, 2010; Accepted August 22, 2010.
This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
Abstract
Background
Fucoidan is a sulfated polysaccharide found in brown algae; it has been shown to exhibit a number of biological effects, including anti-tumor effects. In this study, we evaluated the effects of fucoidan on apoptosis in HT-29 and HCT116 human colon cancer cells.
Methods
HT-29 and HCT116 cells were cultured with various concentrations of fucoidan (0 - 20 μg/mL). Apoptosis was assayed via Hoechst staining and Annexin V staining followed by flow cytometric analysis. Western blot analyses and JC-1 staining were conducted to determine the levels of apoptosis-regulating proteins and mitochondrial membrane permeability, respectively.
Results
Fucoidan induced substantial reductions in viable cell numbers and apoptosis of HT-29 and HCT116 cells in a dose-dependent manner. In HT-29 cells, fucoidan also increased the levels of cleaved caspases-8, -9, -7, and -3, and cleaved poly (ADP-ribose) polymerase (PARP) levels. The levels of the X-linked inhibitor of apoptosis protein and survivin were attenuated in the fucoidan-treated cells. Fucoidan was also shown to enhance mitochondrial membrane permeability, as well as the cytochrome c and Smac/Diablo release from the mitochondria. Fucoidan increased the levels of the Bak and truncated Bid proteins, but reduced the levels of Mcl-1. Additionally, fucoidan increased the levels of the tumor necrosis factor-related apoptosis-inducing ligand, Fas and death receptor 5 proteins. The caspase-8 and -9 inhibitors Z-IETD-FMK and Z-LEHD-FMK induced a reduction in fucoidan-mediated apoptosis. Caspase-8 inhibitor inhibited the fucoidan-induced cleavage of Bid, caspases-9 and -3, and PARP.
Conclusion
The findings of this study indicate that fucoidan induces apoptosis in HT-29 and HCT116 human colon cancer cells, and that this phenomenon is mediated via both the death receptor-mediated and mitochondria-mediated apoptotic pathways. These results suggest that fucoidan may prove useful in the development of a colon cancer-preventive protocol.
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