Dear Editor,
Given the gravity of the current situation regarding increasing cancer incidence and the prevalence of chronic disease in the Republic, I wish to respond in some detail to the letter of Dr Susan O’Reilly in IMT (February 14, 2014), in response to Dr Philip Michael’s letter dated January 24, 2014.

Dr O’Reilly states that Dr Michael’s attempt to correlate fluoridation with cancer is fundamentally flawed. I believe the evidence clearly and unequivocally demonstrates otherwise. What is deeply disturbing in this debate is the steadfast determination of public health bodies in this country, and in other fluoridated countries, to continue to support mass fluoridation of the entire population, despite what I see as overwhelming evidence of harm.
In the context of this debate, my response will only address the direct causal association of fluoride with cancer. It should be noted, however, that fluoride is also a significant contributor to a wide range of chronic inflammatory diseases, metabolic disorders and neurological diseases.
The health authorities are either unaware or refuse to acknowledge that Takahashi et al of the University of Tokyo published findings in the Journal of Epidemiology (2001), which reported a significant association between water fluoridation and cancer. Takahashi and research associates undertook regression analysis of cancer incidence rates and water fluoridation in the US, comparing fluoridated and non-fluoridated states.
Of the 36 cancer sites in males and females examined, 23 (69 per cent) were significantly associated with water fluoridation. Among them were cancer of the colon, prostate, brain, pancreas, liver, kidney, gallbladder, urinary bladder, ovarian, bone, Hodgkin’s diseases and non-Hodgkin lymphoma, multiple myeloma and monocytic leukaemia.
The reason given for the higher cancer incidence rates in fluoridated communities was the extended presence of fluoride in plasma and urine and the infusion of fluoride into the brain and other organs.
Recent published cancer data from the island of Ireland examining cancer incidence in non-fluoridated Northern Ireland and fluoridated Republic of Ireland provides remarkable correlation to these findings. According to the All-Ireland Cancer Registry (2011), the risk of developing many of the cancers was higher in the Republic of Ireland than in Northern Ireland.
The risk of non-melanoma skin cancer, melanoma, leukaemia, bladder, pancreas and brain/central nervous system cancers was significantly higher for both sexes in the Republic of Ireland. For men, the risk of prostate cancer was higher in Republic of Ireland and, for women, cancer of the oesophagus and cervix. The highest risk areas for ovarian cancer were also reported in the Republic of Ireland.
The established scientific facts clearly demonstrate that cancer incidence in the Republic of Ireland is far greater than either non-fluoridated northern Ireland or mainland Europe. For example, according to the World Health Organization, the cancer incidence in the Republic of Ireland is 780 per 100,000 compared to the mean cancer incidence for the entire European region of 380 per 100,000.
To put this information in context, in the past 10 years alone, this would correlate to an additional 180,000 people in the Republic of Ireland who have been diagnosed with cancer above the mean EU regional cancer incident rate for the same period. These are startling and alarming differences.
Furthermore, data from Globocan 2008 provide a comparison of cancer incident rates (top 25 cancers) between Ireland and other fluoridated countries internationally and other geographic regions of the world. For the most fluoridated countries internationally, including the RoI, Australia, New Zealand, United States, Canada and Israel, the incidence of cancers, excluding non-melanoma skin cancers, are significantly above the European and world-wide global averages.
Those who argue against the risk of fluoridation often portray a lack of comprehension of the biological mechanisms of toxicity of fluoride on the human body, which directly and indirectly increase the risk of cancer and other diseases. Among these is the direct established role of fluoride in increasing production of G proteins, free radicals, reactive oxygen species and oxidative stress. There is now a vast amount of published scientific data demonstrating that fluoride causes an increase in G proteins, free radical production, reactive oxygen species and oxidative stress.
The role of free radicals in cancer development was identified as far back as 1996 in the European Journal of Cancer. Verschoor ML et al (2013) reported in the journal Cancer and Metabolism that increased production of reactive oxygen species increases cancer cell proliferation, the growth of new capillary blood vessels that tumours need to grow, contributing to enhanced tumour progression and the spread of cancer within the human body.
According to this study, the increased production of free radicals will result in more aggressive cancer proliferation particularly in prostate, ovarian, breast and intestinal cancers.
Similarly, Kensler and Trush (1984) reported that the molecular mechanisms of action of free radicals promote tumour growth, while Copeland (1986) reported that free radicals play a key role in chemical carcinogenesis. Dreher and Junod (1996) similarly concluded that a large body of evidence suggests important roles of oxygen-free radicals in the expansion of tumour clones and the acquisition of malignant properties. In view of these facts, they concluded that oxygen-free radicals may be considered as an important class of carcinogens.
ROS and oxidative stress have also been implicated in a large range of diseases, including cancer, diabetes, male infertility, autoimmune diseases, atherosclerosis, hypertension and cardiovascular disorders, neurodegenerative diseases (Alzheimer’s disease and Parkinson’s disease), rheumatoid arthritis, and ageing.
In addition, G proteins have been implicated in the pathophysiology of several diseases including, cancer, cardiovascular diseases, hypertension, neuropsychiatric disorders such as alcoholism and schizophrenia, inflammation, asthma, diabetes and endocrine disorders. Over-reactive G proteins are characteristic of some tumours. Activation of G proteins has been identified in adrenal and ovarian tumours and in epidermoid carcinoma.
Equally important is the established role of fluoride as a protoplasmic and enzymatic poison. For example, fluoride stimulates calcitonin production in humans and elevated calcitonin plays a pivotal role in the pathogenesis of many types of cancer, including leukaemia. Apart from the established cancer risk from calcitonin, it is also important to note that research has demonstrated that the fluoride ion inhibits the enzyme arginase. The arginase enzyme metabolizes L-arginine, and L-arginine deficiency has been reported to cause immunosuppression and increase the proliferation of lymphoma cells.
Fluoride is established as an inhibitor or folate metabolism. Studies have demonstrated that folate deficiency has been observed to cause disruption of DNA integrity, DNA strand breaks, chromosomal gaps and breakage, increased uracil misincorporation into DNA, impaired DNA repair and increased mutations, thereby supporting a role for folate deficiencies in carcinogenesis.
Fluoride stimulates the production of haptoglobin and free haptoglobin has been reported to promote, indirectly, carcinogenesis through depression of the immune systems. Haptoglobin expression is characteristic of many types of malignant diseases including breast, cervical and ovarian carcinoma, acute and chronic myeloid leukaemia, and acute lymphoid leukaemia.
Fluoride has also been documented to increase the bioavailability of insulin-like growth factors (IGF-1), thereby contributing to increased cancer risk. Sandhu et al (2002) reported that an increase in IGF-I bioavailability increases the risk of carcinogenesis. Yu and Rohan (2000) reported that IGFs are strong mitogens for a wide variety of cancer cell lines, including sarcoma, leukaemia, and cancers of the prostate, breast, lung, colon, stomach, oesophagus, liver, pancreas, kidney, thyroid, brain, ovary and uterus.
In addition, a number of studies have shown consistently that high circulating levels of IGF-I are associated with increased risk for several common cancers including prostate, breast, lung, colorectal and leukaemia. Yu and Rohan (2000) reported that the level of IGF-binding protein (IGFBP-3) suppresses the mitogenic action of IGF-I, and is inversely associated with the risk of these cancers.
Furthermore, fluoride inhibits leptin secretion, causing overexpression of ghrelin in plasma. Ghrelin is an amino acid peptide hormone that stimulates growth hormone release and has been documented to promote cell growth in breast cancer, prostate cancer and pancreatic adenocarcinoma cancer. Ghrelin expression has also been documented in many endocrine tumour types and hormone-dependent cancers, including testicular tumours.
Overall, I believe it can be concluded that the implications for public health in the Republic from the Department of Health and Irish State initially pursuing such a policy of mass fluoridation in the absence of robust risk assessment, and in continuing to support and implement this policy, have been catastrophic for the general health of this nation.
At the very minimal, the medical community in compliance with the precautionary principle must urgently reassess this policy and seek an immediate cessation to artificial fluoridation in order to protect the health and welfare of future generations. It is my view that continuing such a policy, in light of the overwhelming evidence of harm, is wrong.

Declan Waugh,
Environmental Scientist and Fluoride Researcher

Ireland