ONCE IN BONE, FLUORIDE IS THERE TO STAY
Dr. Richard Sauerheber, Ph.D.
The body deals with fluoride by storing it in the bones. It is said that once the fluoride is in the bones, it is there almost permanently.
However, we all agree that bone is always very slowly being remodeled by osteoclast cells dissolving parts of it by and at the same time by osteoblast cells rebuilding it. This process is well described in The Devil’s Poison by Dean Murphy in his chapter on bone, (pg. 160) especially in the section on osteoporosis, (pgs. 164-169).
Nevertheless, bone fluoride levels that accumulate in individuals who drink fluoridated water and then move to cities that do not have fluoridated water do not drop, even after many years of drinking non-fluoridated water. The NRC 2006 report on fluoride (p. 133) says that the half life of fluoride in bone is twenty years, and this would presume a person is not taking in any new fluoride.
So is fluoride once in bone there to stay, or can it be discharged through “turnover”?
A more complete answer to the question of bone turnover requires looking at both normal and fluorotic bone. Normal bone exhibits significant turnover, where osteoblasts and osteoclasts regularly deposit and remove bone matrix, under regulation by parathyroid hormones, to ensure the calcium concentration in the bloodstream is within a fixed tight normal range. Thus, the main function of bone is to act as a repository for blood calcium ion so that heart function can remain normal even in the presence of dietary calcium deficiency. Indeed, experiments have shown that radioactive phosphate or radioactive calcium injected into the bloodstream are soon found within the bone matrix and this is believed to be due to “turnover” of bone minerals.
However, what does this “turnover” actually mean in principle? If one breaks or cracks a bone, believe me, the bone crack does not turn over and become normal bone, even after waiting an entire lifetime.
To me, the data really indicate that there is no directed turnover, but rather there is exchange of mineral constituents within the bone matrix, where calcium is released during nutritional deficiency and other calcium is re-deposited during calcium sufficiency, which is normal bone metabolism in parts of, but not necessarily all sections and regions, of normal bone. In other words, there is calcium leaving bone and returning to bone, but there is not a complete turnover of all bone material.
Unfortunately, fluoridated bone is in a different category from normal bone because fluoridated bone is abnormal. Fluoridated bone is not mobilized into calcium ion by parathyroid hormone as normal bone is so affected. Further, fluoride consumption causes increased bone mineral deposition and an unnatural increase in replication of osteoblasts. I have always interpreted this to be that the bone tissue is responding to the poisonous insult of the fluoride ion where it does not belong.
After only two years of drinking 1 ppm fluoridated water, the bone fluoride reaches 2,500 mg/kg and after lifetme reaches 4,000 mg/kg or more, and the bone is substantially weakened in stress test experiments because of the fluoride.
It only takes one visit to the San Diego Museum of Man fluorotic bone exhibit to appreciate how hideous and permanent abnormal fluoride in bone really is. Chronic, subacute low level exposure for a lifetime to fluoride causes calcium fluoride spicules, pointy spears, to project out from the bone surface. This is associated in the vertebral column with pinching of the spinal nerve and severe pain and immobilization. It is associated with severe pain in the extremities with prevention of walking. Shorter time duration of exposure leads to lesser effects, where calcium fluoride deposits are present in smaller structures in the bone and on the bone surface. The buildup to larger spicules takes longer of course, but bone ‘turnover’ is useless and helpless to cure or correct or even to mitigate this permanent deformity, much like a broken back stays abnormal with a heal mark even after it is healed, lifetime.
In fluoridated Newburgh, NY the cortical defects in bone caused by fluoride incorporation were not observed ever to become normal again, much like even a normal bone that is broken does not fully re-heal itself over time in spite of “bone turnover”.
Similarly, cells in the brain experience metabolic replacement of intracellular organelles, but yet brain cells do not re-form after one is damaged. Alzheimer’s victims have permanent brain cell deformation and brain cell turnover is again helpless at mitigating the disease.
So it is not incorrect to say that fluoride once deposited into bone is retained essentially permanently. It is theoretically possible that some bone regions, particularly if there were acidic conditions for metabolic reasons, where calcium fluoride might be able to dissolve to some extent, but no evidence of this in the literature exists to my knowledge. Even the fluoride promoting textbook from the 1960’s acknowledges that fluoride accumulates maximal to about 9,000 mg/kg during lifetime consumption of water fluoridated at 1 ppm fluoride ion and makes no claims that it is ever eventually removed. The authors took the position that “fluoride is good”, and therefore that fluoride in bone at this level is somehow “strengthening bone”. The FDA did a full analysis of that claim and decreed that fluoride does not strengthen bone.
Richard Sauerheber, Ph.D.
Michael Powell, D.O.
Rheumatology & Internal Medicine
HOW FLUORIDE AFFECTS BONE
Dear City Council members,
Biochem Biophys Res Commun. 2011 Jun 17. [Epub ahead of print]Sodium fluoride induces apoptosis and alters bcl-2 family protein expression in MC3T3-E1 osteoblastic cells.Yang S, Wang Z, Farquharson C, Alkasir R, Zahra M, Ren G, Han B.SourceCollege of Veterinary Medicine, China Agricultural University, 100193 Beijing, China.AbstractChronic excessive fluoride intake is known to be toxic and can lead to fluorosis and bone pathologies. However, the cellular mechanisms underlying NaF-induced cytotoxicity in osteoblasts are not well understood. The objectives of this study were to determine the effects of fluoride treatment on MC3T3-E1 osteoblastic cell viability, cell cycle analysis, apoptosis and the expression levels of bcl-2 family members: bcl-2 and bax. MC3T3-E1 cells were treated with 10(-5); 5 x10(-5); 10(-4); 5×10(-4) and 10(-3)M NaF for up to 48h. NaF was found to reduce cell viability in a temporal and concentration dependent manner and promote apoptosis even at low concentrations (10(-5)M). This increased apoptosis was due to alterations in the expression of both pro-apoptotic bax and anti-apoptotic bcl-2. The net result was a decrease in the bcl-2/bax ratio which was found at both the mRNA and protein levels. Furthermore, we also noted that NaF-induced S-phase arrest during the cell cycle of MC3T3-E1 cells. These data suggest that fluoride-induced osteoblast apoptosis is mediated by direct effects of fluoride on the expression of bcl-2 family members. Crown Copyright © 2011. Published by Elsevier Inc. All rights reserved.PMID: 21708129 [PubMed – as supplied by publisher]
Thank you for taking this into consideration.