Milk Thistle Monograph

This section is compiled by Frank M. Painter, D.C.
Send all comments or additions to:    Frankp@chiro.org

FROM:   Alternative Medicine Review 1999 (Aug);   4 (4):   272–274 ~ FULL TEXT

Description and Constituents

Silybum marianum (milk thistle) has been used for centuries as an herbal medicine for the treatment of liver disease. Its use for liver disorders dates back to Pliny the Elder, a Roman naturalist, who described milk thistle as being "excellent for carrying off bile." [1] Milk thistle is an annual or biennial plant indigenous to Europe and is also found in some parts of the United States. It grows in rocky soils to a height of three to ten feet with an erect stem that bears large, alternating, prickly-edged leaves. The common name, milk thistle, is derived from the "milky white" veins on the leaves, which, when broken open, yield a milky sap. Flowering season is from June to August, and each stem bears a single, large, purple flower ending in sharp spines. The fruit portion of the plant is glossy brown or grey with spots. [2–4] Silybum marianum contains silymarin, which is composed of the flavanolignans silybin, silydianin, and silychristine, with silybin being the most biologically active. Silymarin is found in highest concentrations in the fruit portion of the plant but is also found in the leaves and seeds. The seeds also contain betaine, trimethylglycine and essential fatty acids, which may contribute to silymarin's hepatoprotective and anti-inflammatory effects.

Mechanisms of Action

Silymarin's hepatoprotective effects are accomplished via several mechanisms including antioxidation, [8] inhibition of lipid peroxidation, [9] enhanced liver detoxification via inhibition of Phase I detoxification and enhanced glucuronidation, [10, 11] and protection of glutathione depletion. [12] Studies have also shown silymarin exhibits several anti-inflammatory effects, including inhibition of leukotriene and prostaglandin synthesis, Kupffer cell inhibition, mast cell stabilization, and inhibition of neutrophil migration. [13–17] In addition, silymarin has been shown to increase hepatocyte protein synthesis, thereby promoting hepatic tissue regeneration. [18] Animal studies have also demonstrated silybin reduces the conversion of hepatic stellate cells into myofibroblasts, slowing or even reversing fibrosis. [19] Clinical studies conducted in Hungary also demonstrated silymarin to have immunomodulatory effects on the diseased liver. [20, 21]

Pharmacokinetics

Silymarin is not water soluble, making tea preparations ineffective; therefore it is usually administered orally in encapsulated form. Because absorption of silymarin from the gastrointestinal tract is only moderate (23–47%), it is best administered as a standardized extract of 70–80 percent silymarin. In animals and humans, peak plasma levels are reached in four to six hours after an oral dose. Silymarin is excreted primarily via the bile but some clearance is also achieved via the kidneys. The clearance half-life of silymarin is six to eight hours. [22, 23]

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