Earlier this week, I came across a study that had hitherto escaped my attention. The study, conducted by a team of French doctors, was published as an abstract last summer in the journal Annals of the Rheumatic Diseases (1).
The study’s findings are very interesting. The authors identified 5 patients in their practice who developed skeletal fluorosis as a consequence of drinking tea (primarily darjeeling tea) over a course of 10 to 25 years. The skeletal fluorosis in these patients was the osteomalacic variety of the disease, in which the bones become softened and weak. As a result of the “fluoride-related osteomalacia,” the patients suffered “spontaneous bone fractures” where their bones fractured without external trauma.
Adding to the significance of this study are the relatively modest amounts of tea that the patients consumed, and the relatively low levels of fluoride found in their bloodstream. The patients consumed between 0.75 to 2 liters per day, and had an average of just 74 parts per billion (ppb) in their blood.
While the blood fluoride levels were measured two days after the patients’ last cup of tea (and thus do not reflect the peak fluoride levels), it is noteworthy that some individuals (particularly people with kidney disease, heart disease, osteoporosis, and combinations thereof) in fluoridated communities can have blood fluoride levels exceeding these levels.
When combining the results of this study, with the results of a similar study published earlier this year in the American Journal of Medicine (2), it is evident that the high fluoride content of many black and green teas is causing bone problems in some members of the population. Unfortunately, it is almost certain that those tea-drinkers suffering from fluoride-induced bone damage are not being correctly diagnosed.
(1) Hayem G, Ballard M, Palazzo E, Somogyi N, Roux F, Meyer O. (2004). Insufficiency bone fractures due to fluorosis in heavy tea drinkers. Annals of the Rheumatic Diseases 63(Suppl 1): 488.
(2) Whyte MP, Essmyer KE, Gannon FH, Reinus WR. (2005). Skeletal fluorosis and instant tea. American Journal of Medicine 118(1):78-82.
Abstract of Study:
Annals of the Rheumatic Diseases July 2004; Supplement 1; Page 488
INSUFFICIENCY BONE FRACTURES DUE TO FLUOROSIS IN HEAVY TEA DRINKERS
G. Hayem, M. Ballard, E. Palazzo, N. Somogyi, F. Roux, O. Meyer
Rheumatology Department, CHU Bichat-Claude Bernard, Paris, France
Background: Fluorosis, whether iatrogenic or endemic, manifests as diffuse hyperostosis, sometimes with features of osteomalacia. In addition to soil, tea is a source of fluoride potentially responsible for fluorosis. Objectives: To describe patients in whom prolonged consumption of large amounts of tea was the only detectable cause of spontaneous bone fractures. Methods: Between 1993 and 2003, we recorded all cases of spontaneous bone fractures with negative findings for classic causes. Each patient was interviewed about dietary habits, including tea consumption. Fluoride levels were assayed routinely in plasma and urine (normal: 5-40 mug/l and .35-.70 mg/d). Results: In 5 of 12 patients (4 females; mean age 63±8 years), each with 1 to 6 spontaneous fractures, fluorosis due to heavy tea drinking was found. Fracture sites included the hip (n=2), calcaneus (n=1), tarsus (n=1), ankle (n=1), and metatarsal bones (n=1). Tea consumption was 750 to 2 liters per day (mainly Darjeeling tea) for 10 to 25 years. Fluoride assays done after at least 48 hours without drinking tea were high in plasma and urine (74.4 ± 29.3 mug/l and .96 ± .45 mg/d, respectively). There were no causes of stress fracture, and tests were negative for other causes of osteoporosis or osteomalacia potentially responsible for insufficiency fractures; in particular, plasma calcium, phosphorus, and 25-hydroxy-cholecalciferol were normal. No past or current treatments known to affect bone metabolism were recorded. In none of the 5 patients did absorptiometry show osteoporosis. Conclusion: Heavy and prolonged consumption of tea may be capable of inducing fluoride-related osteomalacia manifesting as unexpected spontaneous bone fractures.