Artificial light at night: melatonin as a mediator between the environment and epigenome.
Study Goal
The researchers aimed to explore the genetic link between melatonin suppression due to artificial light at night (ALAN) and cancer risks, particularly breast cancer, focusing on epigenetic mechanisms.
Results Summary
The study suggests that melatonin suppression by ALAN may contribute to cancer risks through epigenetic modifications, such as global hypomethylation in oncogenes and local hypermethylation in tumor suppressor genes. It highlights the potential reversibility of these modifications and the need for early detection biomarkers.
Population
General population exposed to artificial light at night, with a focus on breast cancer incidence.
Effective Dosage
Not mentioned
Duration
Not mentioned
Interactions
None mentioned
| Intervention | Direction | Endpoint | Population | Dosage | Impact | Claim # |
|---|---|---|---|---|---|---|
excessive use of artificial light at night (ALAN) | increase | several health problems including cancer | - | - | adverse effects are becoming increasingly evident and associated with | #1 |
ALAN | increase | breast cancer incidents | - | - | increase in breast cancer incidents co-distribute with | #2 |
ALAN | increase | ALAN-induced cancer risks | - | - | melatonin suppression is linked to | #3 |
epigenetic remodelling | neutral | oncogene expression | - | - | relationship between | #4 |
- | increase | oncogenes | breast cancer | - | enhanced global hypomethylation is expected in | #5 |
- | increase | promoter CpG chains of tumour suppressor genes | breast cancer | - | local hypermethylation is recognized in | #6 |
pineal melatonin | neutral | cancer prevalence | - | - | epigenetic modifications mediated by | #7 |
ALAN | neutral | epigenetic modifications | - | reversible | induced epigenetic modifications are | #8 |
The adverse effects of excessive use of artificial light at night (ALAN) are becoming increasingly evident and associated with several health problems including cancer. Results of epidemiological studies revealed that the increase in breast cancer incidents co-distribute with ALAN worldwide. There is compiling evidence that suggests that melatonin suppression is linked to ALAN-induced cancer risks, but the specific genetic mechanism linking environmental exposure and the development of disease is not well known. Here we propose a possible genetic link between environmental exposure and tumorigenesis processes. We discuss evidence related to the relationship between epigenetic remodelling and oncogene expression. In breast cancer, enhanced global hypomethylation is expected in oncogenes, whereas in tumour suppressor genes local hypermethylation is recognized in the promoter CpG chains. A putative mechanism of action involving epigenetic modifications mediated by pineal melatonin is discussed in relation to cancer prevalence. Taking into account that ALAN-induced epigenetic modifications are reversible, early detection of cancer development is of great significance in the treatment of the disease. Therefore, new biomarkers for circadian disruption need to be developed to prevent ALAN damage.