Conjugated linoleic acid (CLA) is a fat found naturally primarily in dairy products such as milk and cheese and ruminant meats such as beef and lamb. CLA has been shown to inhibit breast cancer cell growth and migration in the laboratory. However, population studies have not found a protective effect of high dietary CLA intake, possibly because the cancer-promoting components of dairy products and meat outweigh the potential benefits of their CLA content.
The predominant form of CLA in dairy products and meat is the c9,t11 isomer, whereas CLA supplements typically contain a mixture of the c9,t11 and t10,c12 isomers. However, t10,c12-CLA has been found to promote mammary tumor development in animal experiments. Now a new study has reported that t10,c12-CLA stimulates mammary gland development and mammary tumor growth independently of estrogen via an insulin-like growth factor-I (IGF-1) receptor-dependent mechanism.
Types of CLA
Conjugated linoleic acid normally contains a mixture of various isomers of linoleic acid. CLA isomers all have the same molecular formula, but are different structurally and may have somewhat different chemical properties. The major natural CLA isomer is 18:2 cis-9, trans-11 linoleic acid (c9, t11-CLA). Chemically synthesized CLA is a popular supplement used primarily to reduce body fat accumulation. However, such supplemental CLA normally consists of both c9, t11-CLA and t10,c12-CLA (referred to on some supplement labels as Trans-10, Cis-12).
Dietary sources of CLA
The richest sources of CLA are milk, cheese, and butter, as well as meat from ruminants such as cattle, sheep and goats. However, we do not recommend any of these foods for breast cancer survivors or those at high risk for the disease. Those who wish to increase their CLA intake are better off consuming kefir, yogurt, and white button mushrooms, all of which are good dietary sources of CLA, as well as having been found to be associated with lower risk of breast cancer. CLA supplements should be avoided.
Latest research finds t10,c12-CLA promotes mammary tumors in mice
The study referenced at the beginning of this news article was designed to investigate the influence of t10,c12-CLA on mammary gland development and tumor growth in a mouse model of breast cancer. In the study, the authors report several physiological changes associated with metabolic syndrome in mice on a diet supplemented with t10,c12-CLA. Such supplementation induced high circulating insulin levels in the mice and increased insulin-like growth factor-I receptor expression during mammary gland growth. This effect was confirmed by its reversal upon drug-induced inhibition of insulin-like growth factor-I receptor function.
These changes were found to lead to ovary-independent (i.e., estrogen-independent) development and growth of the mammary ducts. The onset of breast development near puberty is widely believed to be estrogen dependent. However, the estrogen-independence of this CLA-induced mammary gland growth was confirmed by the fact that it also took place in male mice, as well as in female mice with drug-induced inhibition of either estrogen receptor function or aromatase (estrogen biosynthesis). Mammary gland growth stimulated by t10,c12-CLA also increased mammary tumor development in mice that had had their ovaries removed (modeling the postmenopausal state). The authors conclude that metabolic dysregulation induced by t10,c12-CLA stimulates mammary gland growth (independently of ovarian function) by means of an insulin-like growth factor-I receptor-dependent mechanism.