melatonin to fight cancer
Breast cancer supplement strategy - raising Melatonin levels?
Laboratory experiments have found that low levels of melatonin stimulate the growth of
certain types of breast cancer cells. Researchers found adding melatonin to these cells
inhibits their growth. Melatonin is widely recommended because it has several beneficial
methods of action.
•A high number of women with estrogen receptor positive tumors have
low levels of melatonin in their blood.
•Melatonin appears to work as an anti-estrogen on tumor cells. although
differently than Tamoxifen. When the two are combined, the result is better
than Tamoxifen alone. (Lissoni et`al., 1995.)
•A 2006 study showed Melatonin may work as a kind of aromatase
inhibitor. (Cos et al.)
•Low levels of melatonin have been associated with breast cancer
occurrence and development. Women who work predominantly at night
and are exposed to light, which inhibits melatonin production and alters
the circadian rhythm, have an increased risk of breast cancer
development (Schernhammer et al. 2003).
•The circadian rhythm alone is a significant predictor of survival time for
breast cancer patients (Sephton et al. 2000).
• Melatonin demonstrates growth inhibitory effects by inducing
differentiation (“normalizing” cancer cells)(Cos et al. 1996) as well directly
inhibits breast cancer cell proliferation (Ram et al. 2000) and boosting the
production of immune components, including natural killer cells (NK cells)
that have an ability to kill metastasized cancer cells.
Melatonin can be safely taken for an indefinite period of time. The
suggested dose of melatonin for breast cancer patients is 3-50 mg at
bedtime. Some people initially experience vivid dreams or morning
drowsiness. To avoid these minor side effects melatonin may be taken in
low doses nightly and the dose slowly increased over a period of several
weeks. Consult your doctor before starting this or any supplement.
Interesting research on Melatonin
Curr Med Chem. 2010;17(36):4462-81.
Basic mechanisms involved in the anti-cancer effects of melatonin.
Mediavilla MD, Sanchez-Barcelo EJ, Tan DX, Manchester L, Reiter RJ.
Department of Physiology & Pharmacology, School of Medicine, University of Cantabria,
39011 Santander, Spain.
It is commonly accepted that melatonin (N-acetyl-5-methoxytryptamine), the most relevant
pineal secretory product, has oncostatic properties in a wide variety of tumors and,
especially, in those identified as being hormonedependent. The objective of the present
article is to offer a global and integrative view of the mechanisms involved in the oncostatic
actions of this indoleamine. Due to the wide spectrum of melatonin's actions, the
mechanisms that may be involved in its ability to counteract tumor growth are varied. These
include: a) antioxidant effects; b) regulation of the estrogen receptor expression and
transactivation; c) modulation of the enzymes involved in the local synthesis of estrogens; d)
modulation of cell cycle and induction of apoptosis; e) inhibition of telomerase activity; f)
inhibition of metastasis; g) prevention of circadian disruption; h) antiangiogenesis; i)
epigenetic effects; j) stimulation of cell differentiation; and k) activation of the immune
system. The data supporting each of these oncostatic actions of melatonin are summarized
in this review. Moreover, the list of actions described may not be exhaustive in terms of how
melatonin modulates tumor growth.
Epidemiology. 2006 Jan;17(1):108-11.
Night work and risk of breast cancer.
Schernhammer ES, Kroenke CH, Laden F, Hankinson SE.
Channing Laboratory, Department of Medicine, Brigham and Women's Hospital and Harvard
Medical School, Boston, Massachusetts 02115, USA. email@example.com.
BACKGROUND: Melatonin shows potential oncostatic activity and is acutely suppressed by
light exposure. Some evidence suggests an association between night work and breast
cancer risk, possibly through the melatonin pathway. METHODS: In a cohort of
premenopausal nurses, we prospectively studied the relation between rotating night shift
work and breast cancer risk. Total number of months during which the nurses worked
rotating night shifts was first assessed at baseline in 1989 and periodically updated
thereafter. We used Cox proportional hazards models to calculate relative risks (RRs) and
95% confidence intervals (CIs). RESULTS: Among 115,022 women without cancer at baseline,
1,352 developed invasive breast cancer during 12 years of follow up. Women who reported
more than 20 years of rotating night shift work experienced an elevated relative risk of
breast cancer compared with women who did not report any rotating night shift work
(multivariate RR = 1.79; 95% CI = 1.06-3.01). There was no increase in risk associated with
fewer years of rotating night work. CONCLUSION: Our results suggest a modestly elevated
risk of breast cancer after longer periods of rotating night work. Additional studies are
warranted to rule out small sample size or uncontrolled sources for confounding as
Melatonin increases the survival time of animals with untreated mammary tumours:
Saez MC, Barriga C, Garcia JJ, Rodriguez AB, Masot J, Duran E, Ortega E.
Department of Physiology, Faculty of Science, University of Extremadura, Badajoz, Spain.
The aim of this study was to evaluate the therapeutic effect of melatonin, the main hormone
of the pineal gland, on rats with advanced and untreated mammary tumours. Mammary
tumours were chemically induced in Sprague-Dawley rats with the carcinogen 9,10-dimethyl-
1,2-bezanthracene (DMBA). After the appearance of tumours the effect of melatonin (5 mg/ml
per rat per day) was then evaluated on the survival time, tumour multiplicity, and tumour
volume until the death of the animals. In addition, the variations in prolactin, noradrenaline
and adrenaline concentrations, and in the percentage of NK cells were evaluated after one
month of the treatment with melatonin. Daily administration of melatonin increased
significantly the survival time of tumour-bearing animals (p<0.05 with respect to the control
non-melatonin-receiving rats). The increased survival time did not correlate, however, with
changes in either tumour multiplicity or tumour growth rate. Animals with mammary tumours
exhibited an increase (p<0.05 with respect to healthy animals) in prolactin and
catecholamine concentrations. The administration of melatonin stabilized the hormone
levels, returning them to those in the basal-healthy animals. Rats with mammary tumours
also presented lower percentages of NK cells, which were not increased by the
administration of melatonin. The results strongly suggest that melatonin per se is beneficial
during advanced breast cancer. It increases survival time, maybe by improving the
homeostatic and neuroendocrine equilibrium which is imbalanced during advanced breast
Int J Cancer. 2006 Jan 15;118(2):274-8.
Melatonin inhibits the growth of DMBA-induced mammary tumors by decreasing the local
biosynthesis of estrogens through the modulation of aromatase activity.
Cos S, Gonzalez A, Guezmes A, Mediavilla MD, Martinez-Campa C, Alonso-Gonzalez C,
Department of Physiology and Pharmacology, School of Medicine, University of Cantabria,
Melatonin inhibits the growth of breast cancer cells by interacting with estrogen-responsive
pathways, thus behaving as an antiestrogenic hormone. Recently, we described that
melatonin reduces aromatase expression and activity in MCF-7 human breast cancer cells,
thus modulating the local estrogen biosynthesis. To investigate the in vivo aromatase-
inhibitory properties of melatonin in our current study, this indoleamine was administered to
rats bearing DMBA-induced mammary tumors, ovariectomized (ovx) and treated with
testosterone. In these castrated animals, the growth of the estrogen-sensitive mammary
tumors depends on the local aromatization of testosterone to estrogens. Ovariectomy
significantly reduced the size of the tumors while the administration of testosterone to ovx
animals stimulated tumor growth, an effect that was suppressed by administration of
melatonin or the aromatase inhibitor aminoglutethimide. Uterine weight of ovx rats, which
depends 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 depend 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 the uncastrated. We conclude that melatonin could exert its antitumoral
effects on hormone-dependent mammary tumors by inhibiting the aromatase activity of the