Melatonin: A Hormone That Protects Against Breast Cancer and Aging

Thursday, April 10, 2008 by: Barbara L. Minton
Tags: melatonin, health news, Natural News

(NewsTarget) Melatonin is nature's sleeping pill. It is secreted by the light sensitive pineal gland which regulates our biological clock and synchronizes our hormonal-immune network. Our level of melatonin rises with darkness and falls with light. According to Dr. Uzzi Reiss, in his book Natural Hormone Balance, a healthy pineal gland produces 2.5 milligrams of melatonin every twenty-four hours.

Melatonin plays a central role in the natural aging processes of the body. When pineal production begins to diminish, at around age 40, the decline sets off changes in the operation of the body's cells. The physiology of the cell shifts from repair and rejuvenation to aging and degeneration.

Recent studies are now showing that as our levels of melatonin sink, our chances for breast cancer rise. Many women with breast cancer have lower levels of melatonin than those without the disease. Laboratory experiments indicate that lower levels of melatonin stimulate growth of breast cancer cells. Adding melatonin to these cells inhibits their growth.

Breast cancer and melatonin: studies and results

According to a study at the Department of Physiology, Faculty of Science, University of Extremadura, Badajoz, Spain, published in Molecular and Cellular Biochemistry, Oct. 2005, melatonin increases the survival time of animals with untreated mammary tumors.

The aim of the study was to evaluate the therapeutic effect of melatonin on rats with advanced and untreated mammary tumors. Mammary tumors were chemically induced in rats. Following appearance of the tumors, the effect of melatonin was evaluated based on the survival time, tumor multiplicity, and tumor volume up until the death of the animals. Additionally, the variations in prolactin, noradrenaline and adrenaline concentrations, and percentage of NK cells were evaluated after one month of the melatonin treatment.

Results indicate that daily administration of melatonin increased significantly the survival time of tumor bearing animals compared to the control non-melatonin receiving rats. However, the lengthened survival time did not correlate with changes in either tumor multiplicity or growth rates. Animals with mammary tumors exhibited increased levels of prolactin and catecholamine concentrations compared to the healthy animals. The administration of melatonin stabilized the hormone levels, returning them to the levels of the healthy animals. Rats with mammary tumors also presented lower percentages of NK cells, however these levels were not increased with the administration of melatonin. Researchers concluded that melatonin is beneficial during advanced breast cancer. It increases survival time, perhaps by improving the homeostatic and neuroendocrine equilibrium which is imbalanced during advanced breast cancer.

As published in the International Journal of Cancer, January, 2006, researchers at the Department of Physiology and Pharmacology, School of Medicine, University of Cantabria, Santander, Spain, found that melatonin inhibits the growth of induced mammary tumors by decreasing the local biosynthesis of estrogens through the modulation of aromatase activity. They note that melatonin inhibits the growth of breast cancer cells by interacting with estrogen-responsive pathways, effectively behaving as an anti-estrogenic hormone. They had previously described that melatonin reduces aromatase expression and activity in human breast cancer cells, thus modulating local estrogen biosynthesis.

To investigate the in vivo aromatase-inhibitory properties of melatonin in the current study, the indoleamine was administered to rats bearing induced mammary tumors ovariectomized and treated with testosterone. In these castrated animals, the growth of the estrogen-sensitive tumors depended on the local aromatization of testosterone to estrogens. Ovariectomy significantly reduced the size of the tumors while the administration of testosterone to ovariectomized animals stimulated tumor growth, an effect that was suppressed by administration of melatonin or the aromatase inhibitor aminoglutethimide. Uterine weight of the rats, which depended on the local synthesis of estrogens, was increased by testosterone, except in those animals that were also treated with melatonin or aminoglutethimide. The growth-stimulatory effects of testosterone on the uterus and tumors depended exclusively on locally formed estrogens, since no changes in serum estradiol were appreciated in testosterone treated rats.

Tumors from animals treated with melatonin had lower microsomal aromatase activity than tumors of animals from other groups, and incubation with melatonin decreased the aromatase activity of microsomal fractions of tumors. Animals treated with melatonin had the same survival probability as the castrated animals and significantly higher survival probability than those not castrated.

Researchers conclude that melatonin could exert its antitumoral effects on hormone dependent mammary tumors by inhibiting the aromatase activity of the tumoral tissue.

And in the April, 2007 edition of Oncology Report, this same research team at the University of Cantabria, Santander, Spain, reports the effects of MT1 melatonin receptor over-expression on the aromatase-suppressive effect of melatonin in human breast cancer cells. They note that a major mechanism through which melatonin reduces the development of breast cancer is based on its anti-estrogenic actions by interfering at different levels with the estrogen-signaling pathways.

Transfection of the MT1 melatonin receptor in the breast cancer cells significantly decreased aromatase activity, and MT1-transfected cells showed a level of aromatase activity that was 50% of vector-transfected cells. The proliferation of estrogen-sensitive cells in an estradiol-free media but in the presence of testosterone (an indirect measure of aromatase activity) was strongly inhibited by melatonin in those cells over-expressing the MT1 receptor. This inhibitory effect of melatonin on cell growth was higher on MT1 transfected cells than in vector transfected cells. In MT1-transfected cells, aromatase activity was inhibited by melatonin. The same concentrations of melatonin did not significantly influence the aromatase activity of the vector-transfected cells. MT1 melatonin receptor transfection induced a 55% inhibition of aromatase expression in comparison to vector-transfected cells. Additionally, in MT1-transfected cells, melatonin treatment inhibited aromatase expression and induced a higher down-regulation of aromatase expression than in vector-transfected cells.

The researchers concluded that their findings point to the importance of the MT1 melatonin receptor in mediating the oncostatic action of melatonin in human breast cancer cells, and confirm the MT1 melatonin receptor as a major mediator in the melatonin signaling pathway in breast cancer.

Supplementing with melatonin

Since production of melatonin by the pineal gland begins to decline at age 40, it follows that anyone over the age of 40 may be melatonin deficient and may benefit from supplementation as a preventative. Since melatonin is produced while you sleep, it also follows that if you do not get enough sleep, your levels of melatonin may be deficient. Enough sleep is 8 or more hours. Supplementing with melatonin may also be indicated for those who now have or once had breast cancer.

Your melatonin level can be measured with a simple blood test.

According to Dr. Reiss, you should not take melatonin if you have exhausted adrenal glands, symptomized by constant fatigue, low blood pressure, feeling faint when standing up, and low tolerance for physical and emotional stress. Melatonin can reduce the production of cortisol and would be contraindicated for this condition. When adrenal glands are again healthy, supplementation can be started. Women who are trying to conceive should not take melatonin as it could negatively impact the ovulation process.

Melatonin supplements are synthesized to be bio-identical with your own melatonin. They are available at health food stores in capsules, sublingual drops, pills, and as an oral spray.

For anti-aging, Dr. Reiss recommends starting with 0.25 to 0.5 milligrams and increasing the dose gradually until you notice a side effect. The optimal dose is usually 1 to 5 milligrams.

Side effects from excess melatonin are drowsiness upon waking, wild dreams that are not pleasant, waking up nervous, sweating, or with palpitations, and decreased estrogen and progesterone levels.

There is disagreement among authorities as to whether higher doses of melatonin should be recommended for cancer prevention. Dr. Reiss recommends 20 to 40 milligrams daily for prevention. He notes that participants in studies using these very high doses did not develop the side effects seen at lower doses.

Dr. John Lee, in his book What Your Doctor May Not Tell You About Breast Cancer, says that high melatonin levels reduce the ovarian production of estrogens and progesterone, and this is the feedback that is thought to be protective against breast cancer. However, he stresses that all the body's hormones must be in balance, and more is not better when it comes to melatonin. He recommends supplementing with no more than 1 milligram of melatonin sublingually just before bedtime.

If you choose to rely on you own production of melatonin, be aware that production of melatonin rises from bedtime until the middle of the night, and then slowly declines throughout the rest of the night. This production is dependent on you sleeping in a dark room. If you get up during the night and turn on the light or open the refrigerator door, your melatonin production will abruptly stop.

About the author

Barbara is a school psychologist, a published author in the area of personal finance, a breast cancer survivor using "alternative" treatments, a born existentialist, and a student of nature and all things natural.