The epidemic of obesity and changes in food intake: the Fluoride Hypothesis

Physiol Behav. 2004 Aug;82(1):115-21. doi: 10.1016/j.physbeh.2004.04.033.


The epidemic of obesity is worldwide. It will be followed by an epidemic of diabetes. Although there is a genetic basis for obesity and diabetes, the current epidemic reflects the failure of our ancient genes to cope with a modern toxic environment. To put it another way, the genetic background loads the gun, but the environment pulls the trigger. Diet, lifestyle and exercise are the cornerstones of current approaches to treating obesity. However, these approaches that depend on individuals making lifestyle changes have been ineffective in preventing the epidemic. An alternative model views obesity as an epidemiological disease with food(s) and other environmental agents acting on the host to produce disease. The consumption patterns for many foods have changed over the past 30 years, but the increase in the consumption of high-fructose corn syrup (HFCS) for soft drinks is far and away the largest. Moreover, the rise in HFCS intake is an environmental insult that has occurred at exactly the same time as obesity began to increase in prevalence. Rising soft drink consumption is associated with a decrease in milk consumption and a decrease in calcium intake, which has an inverse relationship to body mass index (BMI). To combat the epidemic of obesity, we need new strategies that flow from the epidemiological model. The Fluoride Hypothesis for obesity proposes that we can make environmental changes that when made, will reduce the epidemic of obesity, in much the same way as fluoride reduced the incidence of dental disease. Fluoride-like strategies can work without the personal effort required by changes in lifestyle. In this context, fluoride is also an acronym for treatment and prevention of obesity: For Lowering Universal Obesity Rates are Implement ideas that Don't demand Effort (FLUORIDE).

Publication types

  • Review

MeSH terms

  • Animals
  • Appetite Regulation / drug effects
  • Appetite Regulation / physiology
  • Diabetes Mellitus, Type 2 / epidemiology
  • Diabetes Mellitus, Type 2 / physiopathology
  • Eating / drug effects*
  • Eating / physiology
  • Fluorides / adverse effects*
  • Fructose / administration & dosage
  • Fructose / adverse effects
  • Fructose / metabolism
  • Humans
  • Models, Biological
  • Obesity / chemically induced*
  • Obesity / epidemiology*
  • Sweetening Agents / administration & dosage
  • Sweetening Agents / adverse effects


  • Sweetening Agents
  • Fructose
  • Fluorides