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Showing posts with label fluoridated water. Show all posts
Showing posts with label fluoridated water. Show all posts

Monday, March 25, 2013

More Risks From Fluoride

Heavy tea drinkers getting skeletal fluorosis.  The risk is much higher where water is artificially fluoridated with fertilizer waste products containing fluorsilicic acid.  This also gives you lead, mercury, arsenic and a wide range of other toxic heavy metals.  Places like Seattle and Everett along with many other Washington state communities are exposed daily to these poisons and the state health department endorses the actions.  Phoenix and many Arizona locations also are subjected to artificial fluoridation and seem to be beholden to Delta Dental's PR hype.  
Happily people are wising up and saying no, learn more about the risk of fluoridation at FluorideAlet.org

Be aware that green tea is a high fluoride source and it can lead to pancreatic cancer.
Selections from Natural Health News  - 30+

Jul 22, 2011
If you follow this blog and our other web work you may know that I have frequently spoken out against green tea, especially as it is marketed to be the panacea of the world. I do drink green tea from time to time, but very ...
Feb 11, 2009
"We know that cancer patients look to green tea extracts among other natural supplements to complement their therapeutic regimens," Dr. Axel Schonthal, said in a statement. "We wanted to better understand how the ...
Apr 04, 2011
This and previous research suggests that consuming green or oolong tea is associated with lower serum folate levels in pregnant women. Given the potential adverse effects of folate deficiency on fetal malformations such as ...
Apr 05, 2011
You might think of fluoridated water as a good thing—after all, this organic compound is added to our drinking supply for a reason, right? Unfortunately, however, the bigger picture isn't quite so clear: Although water ...
May 02, 2012
I am sure Mary also is blind to the damage caused by fluoride as it is forced on thousands of Washington State citizens without their permission in the form of toxic and heavy metal laden fertilizer waste provided by Cargill.
Jul 08, 2011
Watch for fluoride is prescription drugs like antibiotics (fluorquinolones) and antidepressants (SSRI,SNRI) , as well as others. Many foods like soy and others sprayed with pesticides and herbicides contain fluoride too.
Jan 11, 2011
The New York Times just reported that a "political battle" is brewing on EPA's decision to phase out the use of sulfuryl fluoride as a food fumigant in the US. According to the Times, Senator James Inhofe (R-Okla.) wants to ...

Sunday, March 07, 2010

New fluoride-lead study cause for ending fluoridation

A very important new study has just been published, ahead of print, by the journal Toxicology, in February 2010:

Fluoride increases lead concentrations in whole blood and in calcified tissues from lead-exposed rats

By Sawana RMM (a), Leite GAS (a), Saraiva MCP (a), Barbosa Jr. F (b), Tanus-Santos JE (c), Gerlach RF (a)

(a) School of Dentistry of Ribeirao Preto, University of Sao Paulo
(b) School of Pharmaceutical Sciences of Ribeirao Preto, University of Sao Paulo
(c) Faculty of Medicine of Ribeirao Preto, University of Sao Paulo

The authors note that, "Higher blood lead levels have been reported in children living in communities that receive fluoride-treated water." They cite the two papers on Masters and Coplan (1999, 2000).

The authors designed an animal experiment to see whether fluoride co-administered with lead increases lead concentrations in blood and calcified tissues. It is important to note that the fluoride compound that they used was hexafluorosilicic acid, one of the silicon fluorides used as fluoridating agents in over 90% of the water supplies fluoridated in the US. Hitherto, nearly all animal experiments have used sodium fluoride.

METHOD: Four groups (i.e. a control group; a fluoride group; a lead group; a fluoride plus lead group) of female (Wistar) rats and their offspring were exposed to different drinking water preparations from 1 week prior to mating until offspring were 81 days old. The drinking water preparations used in the four groups were:
1) The Control Group received water containing maximally 0.1mg/L of fluoride and 0.5 µg/L of lead.

2) The Fluoride group (the F group) received water containing 100mg/L of fluoride (administered as hexafluorosilicic acid)

3) The Lead group (the Pb group) given 30mg/L of lead (administered as lead acetate)

4) The Combined Lead and Fluoride group (the F + Pb group) given 100mg/L of fluoride as hexafluorosilicic acid and 30mg/L of lead as lead acetate

Blood and calcified tissues (enamel, dentine, and bone) were harvested at day 81 for lead and fluoride analyses.

RESULTS: Higher blood lead concentrations (over three times) were found in the fluoride plus lead group compared with the lead group (76.7+/-11.0mug/dL versus 22.6+/-8.5mug/dL, respectively; p<0.001)." Two- to 3-fold higher lead concentrations were found in the calcified tissues in the fluoride plus lead group compared with the lead group (all p<0.001). Lead concentrations were found to be 2.5 times higher in the superficial enamel, 3 times higher in surface bone, 2 times higher in whole bone, and 1.7 times higher in the dentine when the animals were co-exposed to fluoride, thus indicating a consistent rise in the amounts of lead found in whole blood and calcified tissues in the F+Pb Group. CONCLUSIONS: The authors concluded: "These findings show that fluoride consistently increases blood lead and calcified tissues lead concentrations in animals exposed to low levels of lead and suggest that a biological effect not yet recognized may underlie the epidemiological association between increased blood lead levels in children living in water-fluoridated communities." Probably anticipating the usual criticism leveled against animal studies of this type by pro-fluoridation zealots, the authors of this study carefully address the issue of the concentrations of both lead and fluoride used in this experiment. They write:
The concentration of lead in drinking water used in the present study is considered a low concentration for rodents (Leasure et al., 2008). However, while the fluoride concentration used in the present study could be considered relatively high for rodents (100mg/L or ppm), this concentration was chosen because it produces plasma fluoride levels that are comparable with those commonly found in humans chronically exposed to 8mg/L of fluoride in the drinking water, which is a concentration known to cause severe fluorosis.

Since this study was based on a hypothesis derived from epidemiological evidence from thousands of children (that fluoride from the water might increase BPblevels), we felt that we had to maximize fluoride concentrations to observe its influence on lead levels in this proof-of-concept animal study. Although children are not chronically exposed to high concentrations of fluoride (100ppm) by means of drinking/cooking water, children are frequently exposed to high levels of fluoride during their first years because of the many sources of fluoride available to them. Since fluoride is not considered a toxic agent, it is widely available through mouth rinses, toothpastes, tablets, besides the fluoride present in drinking water, beverages, and food. Indeed, the widespread presence of fluoride increased the prevalence of fluorosis in the USA (Pendrys, 2000) and in other countries (Leverett, 1986; Jackson et al., 1999; Tabari et al.,2000; Tsutsui et al.,2000; Pereira et al.,2000). Therefore, it is likely that young children may experience episodes of exposure to high levels of fluoride, which may cause their BPb (blood lead) levels to increase and produce more lead toxicity.

A reason for major concern is the fact that exposure to increased amounts of lead and fluoride occurs at about the same age (1-3 years). Some studies of fluorosis prevalence point to a higher degree of fluorosis in front teeth and first molars (Ismail et al., 1990), which is an indirect measure of dose that indicates that the children receive the highest fluoride doses when their front teeth and first molars mineralize(at ages 1-5 years). This is about the same time when BPb levels are the highest in children. Infact, the exposure of children to lead apparently peaks at 12-36 months of age, which is the time when toddlers experience prominent hand-to-mouth behavior (Binns et al., 2007). Therefore, this is a critical time when systemic exposure to fluoride should be minimized, since fluoride may increase lead accumulation, and any preventable exposure to lead should be avoided (Binns et al., 2007).
FAN's comment: In essence these authors have provided a well-designed animal study supporting the epidemiological findings of Masters and Coplan.

No one can deny that even very low levels of lead exposure can compromise the intellectual development and behavior of young children. If, as this experiment shows in animals, and Masters and Coplan may have found in epidemiological studies, that lead exposure (from any source) is increased by the presence of fluoride in the water, in any rational world this should force the end of fluoridation immediately. What parent in their right mind would knowingly allow the possibility that their child's mental development be impaired in exchange for some slight and questionable benefit to their teeth. However, without the mainstream media and the majority of environmental organizations involved in this issue it is hard to get this information to parents. Thus the chances are that this study will be ignored, like the landmark NRC (2006) review, by those governments determined to continue fluoridation whatever the costs to public health.

As each new scientific study makes the practice of water fluoridation more and more unjustified one feels as if one is caught up in some Kafka novel. We are trapped by a text that was written in 1950 when the US Public Health Service endorsed fluoridation with practically no science on the table. This endorsement set off such a cascade of endorsement dominoes from "professional" bodies that no one seems to have the guts to say was a terrible mistake. All one's efforts to point out - like the little boy in Hans Christian Anderson's famous tale - that the emperor has no clothes are met by derision by the modern day courtiers at the CDC and the ADA. Science has been subordinated to authority and public policy has become the plaything of the arrogant.

Meanwhile, for those who care for their common man this study is another critically important piece of ammunition in the battle to end this sordid practice worldwide.

The abstract of the paper can be accessed at http://www.ncbi.nlm.nih.gov/pubmed/20188782?itool=Email.EmailReport.Pubmed_ReportSelector.Pubmed_RVDocSum&ordinalpos=6

Saturday, January 10, 2009

Alzheimer's drugs double death risk

Use of Fluoride containing anti-psychotics included in this study. Another issue to consider above most for problems with Alzheimer's disease.

Fluoride suppresses proper function of the thyroid gland. As I have mentioned elsewhere, 67% of people in Alzheimer's care facilities in 1998 had a thyroid disorder. Anyone on long term use of a fluoride containing drug, in an area where fluoride is forced into the municipal water system, is already on fluoride overload.

I guess I wonder where are those asking the right questions...
Alzheimer's drugs double death risk in elderly
By MARIA CHENG, AP Medical Writer
Thu Jan 8, 2009

LONDON – Anti-psychotic drugs commonly used to treat Alzheimer's disease may double a patient's chance of dying within a few years, suggests a new study that adds to concerns already known about such medications.

"For the vast majority of Alzheimer's patients, taking these drugs is probably not a worthwhile risk," said Clive Ballard, the paper's lead author, of the Wolfson Centre for Age-Related Diseases at King's College London.

"Would I want to take a drug that slightly reduced my aggression but doubled my risk of dying? I'm not sure I would," Ballard said.

The research was published Friday in the medical journal, Lancet Neurology.

Alzheimer's disease is the most common cause of dementia and causes symptoms including aggression, delusions and hallucinations. Previous studies have shown anti-psychotic drugs, which can help control the aggression and hallucinations for a few months raise the risk of death in older patients with dementia. There are other side effects, including respiratory problems and stroke.

Ballard and colleagues followed 165 patients aged 67 to 100 years with moderate to severe Alzheimer's disease from 2001 to 2004 in Britain. Half continued taking their anti-psychotic drugs, which included Risperdal, Thorazine and Stelazine. The other half got placebos.

Of the 83 receiving drugs, 39 were dead after a year. Of the 82 taking fake pills, 27 were dead after a year. Most deaths in both groups were due to pneumonia.

After two years, 46 percent of Alzheimer's patients taking the anti-psychotics were alive, versus 71 percent of those not on the drugs. After three years, only 30 percent of patients on the drugs were alive, versus 59 percent of those not taking drugs.

In the United Kingdom and the United States, guidelines advise doctors to use anti-psychotic drugs cautiously and temporarily. But in many nursing homes in Europe and North America, up to 60 percent of patients with dementia are routinely given the drugs for one to two years.

"The drug regimen for any person with Alzheimer's needs to be personalized," said William Thies of the Alzheimer's Association in the U.S. Thies was not connected to the study. "At some points, some people will be better off with no medication."

Simon Lovestone of the Institute of Psychiatry at King's College in London said psychiatrists should try environmental or behavioral therapies instead of anti-psychotics.

Experts aren't sure how the anti-psychotics increase patients' risk of dying. But they think the drugs could be damaging to the brain and their sedative effects make patients less able to exercise and more susceptible to deadly infections.

The study was paid for by the U.K. Alzheimer's Research Trust. Ballard reported receiving grants from various pharmaceutical companies which make drugs used to treat Alzheimer's patients.
___

On the Net: http://www.lancet.com
Copyright © 2009 The Associated Press. All rights reserved

The Lancet Neurology, Early Online Publication, 9 January 2009
doi:10.1016/S1474-4422(08)70295-3
Longterm Risk of Death for Alzheimer's and Use of Antipsychotics
Editors' note: Antipsychotics do not improve cognitive or neuropsychiatric outcomes in most patients with dementia, and serious concerns have been raised about their side effects in the very old. Increased mortality rate and risk of cerebrovascular events have been reported by previous studies of relatively short duration (usually 12 weeks). In this article, the DART-AD investigators report long-term mortality rates among patients with Alzheimer's disease in residential care after 12-months of neuroleptic treatment, adding to the growing evidence against the use of antipsychotics in this vulnerable population.

The dementia antipsychotic withdrawal trial (DART-AD): long-term follow-up of a randomised placebo-controlled trial.

Original Text: Clive Ballard MD a , Maria Luisa Hanney PhD b, Megan Theodoulou MRCPsych c, Simon Douglas BSc d, Rupert McShane MRCPsych e, Katja Kossakowski BSc a, Randeep Gill MBBS a, Edmund Juszczak MSc f, Ly-Mee Yu MSc f, Robin Jacoby DM c, for the DART-AD investigators

Background: Data from 12-week placebo-controlled trials have led to mounting concerns about increased mortality in patients with Alzheimer's disease (AD) who are prescribed antipsychotics; however, there are no mortality data from long-term placebo-controlled trials. We aimed to assess whether continued treatment with antipsychotics in people with AD is associated with an increased risk of mortality.

Methods: Between October, 2001, and December, 2004, patients with AD who resided in care facilities in the UK were enrolled into a randomised, placebo-controlled, parallel, two-group treatment discontinuation trial. Participants were randomly assigned to continue with their antipsychotic treatment (thioridazine, chlorpromazine, haloperidol, trifluoperazine, or risperidone) for 12 months or to switch their medication to an oral placebo. The primary outcome was mortality at 12 months. An additional follow-up telephone assessment was done to establish whether each participant was still alive 24 months after the enrolment of the last participant (range 24—54 months). Causes of death were obtained from death certificates. Analysis was by intention to treat (ITT) and modified intention to treat (mITT).

This trial is registered with the Cochrane Central Registry of Controlled Trials/National Research Register, number ISRCTN33368770.

Findings: 165 patients were randomised (83 to continue antipsychotic treatment and 82 to placebo), of whom 128 (78%) started treatment (64 continued with their treatment and 64 received placebo). There was a reduction in survival in the patients who continued to receive antipsychotics compared with those who received placebo. Cumulative probability of survival during the 12 months was 70% (95% CI 58—80%) in the continue treatment group versus 77% (64—85%) in the placebo group for the mITT population. Kaplan—Meier estimates of mortality for the whole study period showed a significantly increased risk of mortality for patients who were allocated to continue antipsychotic treatment compared with those allocated to placebo (mITT log rank p=0·03; ITT p=0·02). The hazard ratio for the mITT group was 0·58 (95% CI 0·35 to 0·95) and 0·58 (0·36 to 0·92) for the ITT population. The more pronounced differences between groups during periods of follow up longer than 12 months were evident at specific timepoints (24-month survival 46% vs 71%; 36-month survival 30% vs 59%).

Interpretation: There is an increased long-term risk of mortality in patients with AD who are prescribed antipsychotic medication; these results further highlight the need to seek less harmful alternatives for the long-term treatment of neuropsychiatric symptoms in these patients.

Funding: UK Alzheimer's Research Trust.