May 30, 2005
Women with a genetic tendency towards breast cancer have unstable chromosomes. Studies now show that these chromosomes can be stabilized by taking selenium supplements.
About every twenty cases of breast cancer are due to inheritance. Most often, the cause is an innate mutation in the so-called BRCA1 gene, which, under normal circumstances, repairs damage to chromosomes.
If you carry this mutation, you already have a high risk of breast cancer: Approximately 60% will get the disease before they reach 50, and approximately 85% will get it before they reach 70. At the same time, the risk of ovarian cancer is no less than 60%.
It is a despairing situation to be born with this mutation, which presents the affected with difficult decisions. Some prefer to prevent the cancer by having their breasts and ovaries removed at a young age, while others wait and see if they are among the unlucky ones. Those affected must at least think about having the children they want at a young age if they want to retain the opportunity to breastfeed. There is no certainty as to when the disease will strike.
Now, however, a highly interesting Polish study suggests that the risk can be significantly reduced with a simple supplement of selenium. The supplement drastically reduces the frequency of chromosomal damage in women with the congenital defect. This can, if the results hold, buy the vulnerable women time and reduce their risk of instability in the protective chromosomes.
The experiment was carried out at the Pomeranian Academy of Medicine in Szczecin. It was about measuring the amount of mutations – so-called chromosome breaks – on white blood cells, which in the laboratory were exposed to “chemical radiation” in the form of the chemotherapy drug bleomycin.
Two experiments were performed. In one, chromosome breaks were compared in 26 women with and 26 women without the congenital defect. In the first, 0.59 fractures per cell were measured, while women without the defect had only 0.39.
35 other women, all of whom were carriers of the mutation, now participated in the second trial. Half of them received a daily supplement of approx. 280 mcg selenium a day, after which they had blood samples taken after 1-3 months, so that their blood cells could also be exposed to bleomycin. The result was almost exactly as in the first experiment: In the blood cells of the women who did not receive selenium, 0.63 chromosome breaks occurred per cell, while those who received the selenium had only 0.40 fractures per. cell.
In other words, women with the inherited mutation could increase the stability of their chromosomes to normal with something as simple as a daily selenium supplement. The question then is how this is to be interpreted. Does this mean that they also had their cancer risk reduced?
There are many indications of this, but one cannot be sure. Researchers have concluded that hereditary breast cancer is due in part to unstable chromosomes. Others have found that breast cancer patients have clearly more chromosomal abnormalities in their white blood cells than healthy ones. In addition, several experiments have shown a correlation between the susceptibility to cancer in general and the level of chromosome rupture.
In addition, a study of 3,812 workers who were exposed to mutation-promoting substances showed that those who had the most chromosomal abnormalities were also most likely to get cancer later on. The clues are many.
Selenium has an antioxidant effect and has been shown to be strongly anti-cancer in several trials. As the soil in Poland (just like Denmark) is very low in selenium, the researchers believe that a similar experiment in other countries could give a different result.
The participants received the equivalent of approx. three regular selenium tablets with organic selenium a day. It is a dose that certainly does not exceed what is allowed.
By: Vitality Council
Kowalska E. et al. Increased rates of chromosome breakage in BRCA1 carriers are normalised by oral selenium supplementation. Cancer Epidem Biomarkers Prev 2005;14(5):1302-6.