Human Radiation Effects Group

The Melatonin Hypothesis

Melatonin (N-acetyl-5-methoxytrptamine) is a hormone produced nocturnally in the pineal gland. Its production is triggered by a signal from the eye indicating that light has fallen below ~200 lux. This trigger does not involve the visual system rather recently discovered ganglion cells in the eye (Berson et al. 2002; Hattar et al. 2002). Melatonin is a powerful antioxidant and radical scavenger whose mechanisms of action, some of which are cell receptor mediated, has been extensively researched. As an antioxidant, melatonin acts as a natural anti-cancer agent but it is also known to regulate seasonal breeding in animals and reduced melatonin is associated with depression. The decline in production of melatonin in the aged is associated with the onset of neurodegenerative diseases (see review in Reiter 1998).

Unlike other antioxidants, such as vitamins C and E and glutathione, melatonin enters cells and is able to act directly on DNA. Indeed, the concentration of melatonin in cells, tissues and organs is markedly non-uniform (see Editorial by Reiter 2003). As a result, the so-called normal physiological concentrations of melatonin need to be carefully defined. For example, melatonin concentrations in bile and in the cerebrospinal fluid of the third ventricle are orders of magnitude higher than in the blood.

The nocturnal production of pineal melatonin can be completely suppressed by exposure to light-at-night (LAN). Nowadays, compared to our forefathers, man is exposed to far more LAN, from street and indoor lighting, with a corresponding reduction in the total amount of nocturnal melatonin produced. The so-called melatonin hypothesis (Stevens 1987), postulates that the increased risk in breast cancer in recent decades in industrialised countries results in part from increased exposure to LAN. Strong support for this hypothesis comes from the increased risk of breast cancer in nightshift workers (Swerdlow 2003) and the fact that such workers who go on to contract breast cancer produce lower nocturnal melatonin (Schernhammer & Hankinson 2005). Further support comes from the recent observation that normal physiological concentrations of nocturnal melatonin in women’s blood prevents the growth of human breast tumours when transplanted into rats (Blask et al. 2005).

The melatonin hypothesis has been applied to EMFs (indeed this was integral to the original hypothesis by Stevens, 1987). The adverse health effects ranging from childhood leukaemia through to depression and miscarriage comprises an apparent disparate set of illnesses. However, melatonin suppression or disruption could be a common factor leading to increased risk. Henshaw & Reiter (2005) review the various studies suggesting melatonin disruption by power frequency EMFs. Volunteer experiments involving short-term exposures to magnetic fields (for example, for 30 minutes) tend not to yield evidence of such disruption, although those involving longer terms exposures have shown a clear effect, for example the recent report by Davis et al. (2006). However, studies in animals, in volunteers with comparatively long-term exposures and populations exposed to neighbourhood fields associated with the electricity supply together provides strong evidence of melatonin disruption, including from magnetic fields as low as 0.2 µT. In the case of neighbourhood exposures, it would appear that the effect of switching of magnetic fields and/or of electric fields are an important factor in melatonin disruption. Indeed, the initial volunteer experiments indicating melatonin disruption themselves concerned electric rather than magnetic fields (Wever 1979).

Henshaw & Reiter also hypothesise that melatonin disruption could increase the risk of childhood leukaemia, citing the evidence that melatonin is highly protective of oxidative damage to the human haemopoietic system (Vijayalaxmi et al. 1996) and that in animals melatonin is highly protective of oxidative damage to the fetus (Wakatsuki et al. 1999a, b and 2001; Okatani et al. 1997).

Click here to access the Henshaw & Reiter hypothesis paper "Do magenetic fields cause increased risk of childhood leukaemia via melatonin disruption?"

Updated 22.03.07 by Julie Close