Mobiles double brain cancer risk

Two studies in the leading journal of the Public Library of Sciences suggest  long-term mobile phone use could well be a factor behind the increased incidence of an aggressive type of brain cancer,  glioblastoma. The incidence of this cancer has gone by 34% since the 1990, according to Cancer Research UK.

The first, published this month, exposed glioblastoma  cells to the level of radiation that is consistent with  mobile phone use. The researchers found clear evidence that the mobile phone ‘signal causes transient genetic instability in gliomaderived cells and activates cellular defense systems’.

The second pooled the results of 11 previous studies  and found that long-term use of mobile phones, defined as ten or more years of use, was associated with more than doubling the risk of this type of brain cancer.

Glioblastoma is a particularly aggressive type of brain cancer that has limited  success with conventional treatment, however a ketogenic diet, avoiding all carbohydrates and sugar, is being increasingly reported to be effective as an adjunct to chemotherapy with compelling cases of tumour shrinkage. The ketogenic diet is currently being investigated as a cancer therapy in over a dozen clinical trials.

80 to 90% of the risk of cancer, generally speaking, is due to environmental factors – diet, lifestyle, radiation, chemical and pollution exposure. At most 20% is attributable to genes. This is good news because it means that cancer is largely preventable if you know what the risk factors are.

This new research establishes a mechanism by which mobile phone radiation can cause DNA damage, suggesting that the increasing evidence of an association is of genuine concern.


Al-Serori H et al. ‘Mobile phone specific electromagnetic fields induce transient DNA damage andnucleotide excision repair in serum-deprived human glioblastoma cells.’ PLoSOne. 2018 Apr 12;13(4):e0193677

Yang M, et al  ‘Mobile phone use and glioma risk: A systematic review and meta-analysis.’ PLoS One.2017 May4;12(5):e0175136.