In his latest attempt to win the title of the Internet’s most zealous promoter of water fluoridation, Ken Perrot has done what he accuses his detractors of so often doing; i.e. cherry picking data to support his case. To be fair to Ken, perhaps there is some merit to that charge. In a polarised debate like water fluoridation, both sides tend to fall into that trap. However, for now, let’s focus on Ken’s latest effort and raise the question of why is he not following his own advice and avoiding such blatant distortions?
Ken writes that, “research findings do support a beneficial role of ingested fluoride during teeth development.” Yes, Ken, some do, but surely you are also aware that numerous peer-reviewed articles – at best – cast doubt on the benefits/necessity of ingested fluoride, or – at worst – repudiate the theory entirely. Why have you not mentioned this fact to your readers? Surely a man of your vast knowledge of the fluoridation literature is aware of these articles.
For example, Hellwig & Lennon (2004) write, “a dogma has existed for many decades, that fluoride has to be ingested and acts mainly pre-eruptively. However, recent studies concerning the systemic effect of fluoride supplementation concluded that the caries-preventive effect of fluoride is almost exclusively posteruptive. Moreover, epidemiologists have cast doubt on the validity of the ‘old’ studies dealing with fluoride use.”
Fejerskov (2004) also brought up this issue of the ‘old’ paradigm of the systemic ‘religion,’ which Ken now aims to revive: “When it was thought that fluoride had to be present during tooth mineralisation to ‘improve’ the biological apatite and the ‘caries resistance’ of the teeth, systemic fluoride administration was necessary for maximum benefit. Caries reduction therefore had to be balanced against increasing dental fluorosis. The ‘caries resistance’ concept was shown to be erroneous 25 years ago,” whilst Pizzo et al. (2007) echo similar sentiments: “Several studies conducted in fluoridated and nonfluoridated communities suggested that this method of delivering fluoride may be unnecessary for caries prevention, particularly in the industrialized countries where the caries level has became low.”
In 2009, following a major study, Warren et al. reported, “achieving a caries-free status may have relatively little to do with fluoride intake.” Given the clear disputes over the old systemic belief system, it is little wonder why this research team confirmed, “firmly recommending an “optimal” fluoride intake is problematic.”
More recently, Peckham & Awofeso (2014) reiterated, “it is widely accepted that fluoride only helps prevent dental decay by topical means—by direct action on the tooth enamel predominantly after eruption and dental plaque.”
Why is Ken not telling his readers the other side of the story?
Moreover, whilst the research has been coming in confirming that the old systemic theory is basically a dinosaur, or at least in serious doubt, researchers in non-dental fields have been considering the molecular mechanisms of fluoride toxicity.
For instance, according to Barbier et al. (2010): “Halfway through the twentieth century, fluoride piqued the interest of toxicologists due to its deleterious effects at high concentrations in human populations suffering from fluorosis and in in vivo experimental models. Until the 1990s, the toxicity of fluoride was largely ignored due to its “good reputation” for preventing caries via topical application and in dental toothpastes. However, in the last decade, interest in its undesirable effects has resurfaced due to the awareness that this element interacts with cellular systems even at low doses. In recent years, several investigations demonstrated that fluoride can induce oxidative stress and modulate intracellular redox homeostasis, lipid peroxidation and protein carbonyl content, as well as alter gene expression and cause apoptosis. Genes modulated by fluoride include those related to the stress response, metabolic enzymes, the cell cycle, cell–cell communications and signal transduction.”
This raises the issue of margin of safety, although in the context of necessity, the weight of evidence now reveals the ingestion of fluoride to be a non-essential component of oral health (where the wide availability of topical fluoride applications exists). Ken’s dogged determination to convince his readers of an alternate reality is bizarre, yet equally transparent and disputable, particularly when overall fluoride intakes from multiple sources are considered alongside inadequate population biomonitoring.