Early studies of cartilage's therapeutic potential utilized extracts of bovine (cow) cartilage. The ability of these extracts to suppress inflammation was first described in the early 1960s. The first report that bovine cartilage contains at least one angiogenesis inhibitor was published in the mid-1970s. The use of bovine cartilage extracts to treat patients with cancer and the ability of these extracts to kill cancer cells directly and to stimulate animal immune systems were first described in the mid- to late-1980s.[7,8,9,10]
This complementary and alternative medicine (CAM) information summary provides an overview of the use of milk thistle as a treatment and adjunct agent for people with cancer.
The summary includes a brief history of milk thistle, a review of the laboratory studies and clinical trials, and a description of adverse effects associated with milk thistle use.
This summary contains the following key information:
Milk thistle is a plant whose fruit and seeds have been used for more than 2,000 years...
The first report that shark cartilage contains at least one angiogenesis inhibitor was published in the early 1980s, and the only published report to date of a clinical trial of shark cartilage as a treatment for people with cancer appeared in the late 1990s. The more recent interest in shark cartilage is due, in part, to the greater abundance of cartilage in this animal and its apparently higher level of antiangiogenic activity. Approximately 6% of the body weight of a shark is composed of cartilage, compared with less than 1% of the body weight of a cow. In addition, on a weight-for-weight basis, shark cartilage contains approximately 1,000 times more antiangiogenic activity than bovine cartilage.
As indicated previously (refer to the Overview and General Information sections of this summary for more information), at least three different mechanisms of action have been proposed to explain the anticancer potential of cartilage: 1) it is toxic to cancer cells; 2) it stimulates the immune system; and 3) it inhibits angiogenesis. Only limited evidence is available to support the first two mechanisms of action; however, the evidence in favor of the third mechanism is more substantial (refer to the Laboratory/Animal/Preclinical Studies section of this summary for more information).