Our naturopath had this to say about artemisinin when I asked about the issue of including it in a protocol that is very high in anti-oxidants:

"The body requires both oxidants and anti-oxidants - without oxidants we could not use oxygen. So in the body each group gives signals to the cell which sets up a chain of command. These activities happen independently of each other and do not cancel each other out. The antioxidants will selectively mop up free radicals - if they mopped up all free radicals the body would cease to function as most activity is dependent upon the production of free radicals - including the whole energy cycle which is dominated by the transport of electrons down the electron transport chain. The way the immune system attacks cancer is through oxidant activity.

"Nutritionists have an extremely naive understanding of biophysics and treat the body simply as a biochemical factory. It is not - the transmission caused by any signal in the body occurs as a consequence of a disturbance of the electrical fields.

"As the article [an article that she forwarded us to read] states that "effectiveness of artemisinin is reduced by catalase, dithiothreitol and alpha tocopherol" and that while a diet low in vit E enhanced its activity, those low in selenium made no difference.

"They also found that they could exploit the high iron capacity of cancer cells, iron is a pro-oxidant, to improve the outcome for this agent.

"If you go on to read the article, the authors state that cancer cells are naturally low in all the antioxidant enzyme pathways - merely supplementing with antioxidants does not change the state of the cancer cell. This is why taking massive amounts of antioxidants does not kill cancer - it can only protect the healthy tissues. I have yet to read reports where massive doses vitamin C do kill cancer - but am open to the possibility. We are looking at killing the cancer and the only way that this can occur is through free radical damage generated either by your own immune system, chemotherapy, radiotherapy or the use of herbs that have this activity. With herbs, or course, they do not damage the normal cells."

Comments are welcome!!
Lisa

ARTICLE LINKS:
Fulltext | PDF (229 K)

Dihydroartemisinin inhibits angiogenesis induced by multiple myeloma RPMI8226 cells under hypoxic conditions via downregulation of vascular endothelial growth factor expression and suppression of vascular endothelial growth factor secretion.

PRECLINICAL REPORTS
Anti-Cancer Drugs. 17(7):839-848, August 2006.
Wu, Xiu-Hua a b; Zhou, Hui-Jun a; Lee, Jun a b

Abstract:
Multiple myeloma remains incurable to date; therefore, new biologically target-based therapies are urgently needed. Our previous studies have showed that the antimalarial dihydroartemisinin possessed antiangiogenic activity in solid tumors. The present study evaluated the effect of dihydroartemisinin on human multiple myeloma-induced angiogenesis under hypoxia and elucidated its mechanism of action. An in-vivo chicken chorioallantoic membrane model was used to examine the effect of dihydroartemisinin on multiple myeloma-induced angiogenesis. Compared with conditioned medium of control, conditioned medium from human multiple myeloma RPMI8226 cells pretreated with 3 [mu]mol/l dihydroartemisinin in hypoxia was observed to reduce microvessel growth on chicken chorioallantoic membranes by approximately 28.6% (P<0.05). The level of vascular endothelial growth factor in conditioned medium was determined by enzyme-linked immunosorbent assay. The results confirmed that 3 [mu]mol/l dihydroartemisinin could significantly decrease vascular endothelial growth factor secretion by RPMI8226 cells (P<0.05), which correlated well with the reduction of multiple myeloma-induced angiogenesis on chicken chorioallantoic membranes. Western blot and reverse transcription-polymerase chain reaction results revealed that dihydroartemisinin downregulated the expression of vascular endothelial growth factor in RPMI8226 cells in hypoxia. In addition, we demonstrated that dihydroartemisinin reduced extracellular signal-regulated kinase 1/2 activation and inhibited growth of RPMI8226 cells under hypoxic conditions. Therefore, we concluded that dihydroartemisinin, which is already used to treat malaria and is well tolerated, possesses potential as an antiangiogenic drug in multiple myeloma therapy and thereby may improve patient outcome.

(C) 2006 Lippincott Williams & Wilkins, Inc.