Prozac/Paxil Facts=Same Chemical as Rat Poison

First of all, it needs to be stated that the ‘substance’ referred to as ‘Fluoride’ is a misnomer – there is no such substance listed in the periodic chart of the elements, nor in the prestigious CRC handbook, nor in the sacred ‘bible’ of the pharmaceutical industry – the illustrious ‘Merck Index’. Instead, we find a GAS called Fluorine – and from the use of this gas in various industries such as aluminum manufacturing and the nuclear industry -certain toxic byproducts are created which have ‘captured’ fluorine molecules. One such toxic, poisonous ‘byproduct’ is called sodium Fluoride – which according to the Merck Index is primarily used as rat and cockroach poison and is also the active ingredient in most toothpastes and as an “additive to drinking water”. But sadly, there is much more to this sordid tale.

Did you know that sodium Fluoride is also one of the basic ingredients in both PROZAC (FLUoxetene Hydrochloride) and Sarin Nerve Gas (Isopropyl-Methyl-Phosphoryl FLUORIDE) – (Yes, folks the same Sarin Nerve Gas that terrorists released on a crowded Japanese subway train!). Let me repeat: the truth the American public needs to understand is the fact that Sodium Fluoride is nothing more (or less) than a hazardous waste by-product of the nuclear and aluminum industries. In addition to being the primary ingredient in rat and cockroach poisons, it is also a main ingredient in anesthetic, hypnotic, and psychiatric drugs as well as military NERVE GAS! Why, oh why then is it allowed to be added to the toothpastes and drinking water of the American people?

Historically, this substance was quite expensive for the worlds’ premier chemical companies to dispose of – but in the 50′s and 60′s – Alcoa and the entire aluminum industry – with a vast overabundance of the toxic waste – SOMEHOW sold the FDA and our government on the insane (but highly profitable) idea of buying this poison at a 20,000% markup and then injecting it into our water supply as well as into the nation’s toothpastes and dental rinse. Yes that’s right folks, a 20,000% markup. Consider also that when sodium Fluoride is injected into our drinking water, its level is approximately 1 part-per-million (ppm), but since we only drink ½ of one percent of the total water supply, the hazardous chemical literally ‘goes down the drain’ and voila – the chemical industry has not only a free hazardous waste disposal system – but we have also PAID them handsomely in the process!!

Independent scientific evidence over the past 50 plus years has shown that sodium fluoride shortens our life span, promotes various cancers and mental disturbances, and most importantly, makes humans stupid, docile, and subservient, all in one neat little package. There is increasing evidence that aluminum in the brain is a causative factor in Alzheimer’s Disease, and evidence points towards sodium fluoride’s strong affinity to ‘bond’ with this dangerous aluminum (remember it is a byproduct of aluminum manufacturing) and also it has the ability to ‘trick’ the blood-brain barrier by imitating the hydrogen ion thus allowing this chemical access to brain tissue.

Honest scientists who have attempted to blow the whistle on sodium fluoride’s mega-bucks propaganda campaign have consistently been given a large dose of professional ‘black-listing’ and thus their valid points disputing the current vested interests never have received the ink they deserve in the national press. Just follow the money to find the ‘control’ and you will find prominent American families to be prominent ‘players’ in the scandal. In 1952 a slick PR campaign rammed the concept of ‘fluoridation’ through our Public Health departments and various dental organizations. This slick campaign was more akin to a highly emotional “beer salesman convention” instead of the objective, scientifically researched program that it should have been. It has continued in the same vein right up to the present day – and now sodium fluoride use has now become ‘usual and customary’.

To illustrate the emotional vs. the scientific nature of this issue, just look at the response given by people (perhaps yourself included?) when the subject of fluoridation comes up. You need to ask yourself, “Is this particular response based on EMOTIONS born of TRADITION, or is it truly unbiased and based instead on thoroughly researched objectivity?” There is a tremendous amount of emotional, highly unscientific “know-it-all” emotions attached to the topic of ‘sodium fluoride’ usage -but I personally have yet to find even ONE objective, double blind study that even remotely links sodium fluoride to healthy teeth at ANY AGE.

Instead, I hear and read such blather as “9 out of 10 DENTISTS recommend ‘fluoride’ toothpaste” etc. etc. etc. Let me reiterate: truly independent (unattached to moneyed vested interest groups) scientists who’ve spent a large portion of their lives studying and working with this subject have been hit with a surprising amount of unfair character assassinations from strong vested-interest groups who reap grand profits from the public’s ignorance as well as from their illnesses. (Just follow the money!)

Do you have diabetes and/or kidney disease? There are reportedly more than 11 million Americans with diabetes. If it is true that diabetics drink more liquids than other people, then according to the Physicians Desk Reference these 11 million people are at much higher risk drinking fluoridated water because they will receive a much deadlier dose because of their need for higher than normal water consumption. Kidney disease, by definition, lowers the efficiency of the kidneys, which of course is the primary means in which fluoride (or any other toxic chemical) is eliminated from the body. Does it not make sense that these people shouldn’t drink fluoridated water at all? Cases are on record (Annapolis, Maryland, 1979) where ill kidney patients on dialysis machines died because they ingested relatively small amounts of SODIUM FLUORIDE from unwittingly drinking the ‘fluoridated’ city water supply? Will adequate warnings be given to people with weak kidneys, or will the real cause of such deaths be ‘covered up’ in the name of ‘domestic tranquility’?

Concerning the ‘practice’ of putting sodium fluoride into drinking water, where did this insanity begin and WHO tried it first? From personal research, the very first occurrence of purposefully putting sodium fluoride into drinking water was in the German ghettos and in Nazi Germany’s infamous prison camps. The Gestapo you see had little concern about sodium fluoride’s ‘supposed’ effect on children’s teeth; instead, their reason for mass-medicating water with sodium fluoride was to STERILIZE HUMANS and force the people in their concentration camps into calm, bovine, submission. (See for reference: “The Crime and Punishment of I.G. Farben” written by Joseph Borkin.) Kind of shocking isn’t it folks!! Ah, but it gets even better.

The following letter was received by the Lee Foundation for Nutritional Research, Milwaukee Wisconsin, on 2 October 1954, from a research chemist by the name of Charles Perkins. He writes:

“I have your letter of September 29 asking for further documentation regarding a statement made in my book, “The Truth about Water Fluoridation”, to the effect that the idea of water fluoridation was brought to England from Russia by the Russian Communist Kreminoff. In the 1930′s Hitler and the German Nazis envisioned a world to be dominated and controlled by a Nazi philosophy of pan-Germanism. The German chemists worked out a very ingenious and far-reaching plan of mass-control which was submitted to and adopted by the German General Staff.

This plan was to control the population in any given area through mass medication of drinking water supplies. By this method they could control the population in whole areas, reduce population by water medication that would produce sterility in women, and so on. In this scheme of mass-control, sodium fluoride occupied a prominent place.

“Repeated doses of infinitesimal amounts of fluoride will in time reduce an individual’s power to resist domination, by slowly poisoning and narcotizing a certain area of the brain, thus making him submissive to the will of those who wish to govern him. [A convenient and cost-effective light lobotomy? --- Ott].

“The real reason behind water fluoridation is not to benefit children’s teeth. If this were the real reason there are many ways in which it could be done that are much easier, cheaper, and far more effective. The real purpose behind water fluoridation is to reduce the resistance of the masses to domination and control and loss of liberty.”

“When the Nazis under Hitler decided to go to Poland, both the German General Staff and the Russian General Staff exchanged scientific and military ideas, plans, and personnel, and the scheme of mass control through water medication was seized upon by the Russian Communists because it fitted ideally into their plans to communize the world.”

“I was told of this entire scheme by a German chemist who was an official of the great I.G. Farben chemical industries and was also prominent in the Nazi movement at the time. I say this with all the earnestness and sincerity of a scientist who has spent nearly 20 years’ research into the chemistry, biochemistry, physiology and pathology of fluorine — any person who drinks artificially fluorinated water for a period of one year or more will never again be the same person mentally or physically.”
Signed: CHARLES E. PERKINS, Chemist, 2 October, 1954.

Another letter needs to be quoted at length as well to help corroborate Mr. Perkin’s testimony. This letter was written by a brilliant (and objectively honest) scientist named Dr. E.H. Bronner. Dr. Bronner was a nephew of the great Albert Einstein, served time in a WWII prison camp and wrote the following letter printed in the Catholic Mirror, Springfield, MA, January 1952:

“It appears that the citizens of Massachusetts are among the ‘next’ on the agenda of the water poisoners.

“There is a sinister network of subversive agents, Godless intellectual parasites, working in our country today whose ramifications grow more extensive, more successful and more alarming each new year and whose true objective is to demoralize, paralyze and destroy our great Republic —- from within if they can, according to their plan — for their own possession.”

“The tragic success they have already attained in their long siege to destroy the moral fiber of American life is now one of their most potent footholds towards their own ultimate victory over us.”

“Fluoridation of our community water systems can well become their most subtle weapon for our sure physical and mental deterioration. As a research chemist of established standing, I built within the past 22 years 3 American chemical plants and licensed 6 of my 53 patents. Based on my years of practical experience in the health food and chemical field, let me warn: fluoridation of drinking water is criminal insanity, sure national suicide. DON’T DO IT!!”

“Even in very small quantities, sodium fluoride is a deadly poison to which no effective antidote has been found. Every exterminator knows that it is the most effective rat-killer. Sodium Fluoride is entirely different from organic calcium-fluoro-phosphate needed by our bodies and provided by nature, in God’s great providence and love, to build and strengthen our bones and our teeth. This organic calcium-fluoro-phosphate, derived from proper foods, is an edible organic salt, insoluble in water and assimilable by the human body; whereas the non-organic sodium fluoride used in fluoridating water is instant poison to the body and fully water soluble. The body refuses to assimilate it.”

“Careful, bonafide laboratory experimentation by conscientious, patriotic research chemists, and actual medical experience, have both revealed that instead of preserving or promoting ‘dental health’, fluoridated drinking water destroys teeth before adulthood and after, by the destructive mottling and other pathological conditions it actually causes in them, and also creates many other very grave pathological conditions in the internal organisms of bodies consuming it. How then can it be called a ‘health plan’? What’s behind it?”

“That any so-called ‘Doctors’ would persuade a civilized nation to add voluntarily a deadly poison to its drinking water systems is unbelievable. It is the height of criminal insanity!”

“No wonder Hitler and Stalin fully believed and agreed from 1939 to 1941 that, quoting from both Lenin’s ‘Last Will’ and Hitler’s Mein Kampf: “America we shall demoralize, divide, and destroy from within.”“Are our Civil Defense organizations and agencies awake to the perils of water poisoning by fluoridation? Its use has been recorded in other countries. Sodium Fluoride water solutions are the cheapest and most effective rat killers known to chemists: colorless, odorless, tasteless; no antidote, no remedy, no hope: Instant and complete extermination of rats.”

“Fluoridation of water systems can be slow national suicide, or quick national liquidation. It is criminal insanity ——- treason!!”
Signed: Dr. E.H. Bronner, Research Chemist, Los Angeles

Apparently, the public outcry by Dr. Bronner and others precluded the fluoridation of public water systems for a season – but soon thereafter, the Food and Drug Administration allowed this deadly poison to be put in ‘toothpaste’, and our dentists were systematically brainwashed into providing ‘fluoride treatments’ to their many patients. Of course, today many major metropolitan areas have a minimum of 1 parts per million sodium fluoride systematically added to their water supply and more areas are seeking to add this poison every year. Add to this the fact that bottling companies (soft drinks, juices, etc.) use fluoridated water to make their products – is it any wonder that people can no longer think clearly and ask pertinent questions of their elected and ecclesiastical leaders? Is it also a mystery why so many top Nazi mind control scientists were brought to America by the CIA and their infamous ‘Operation Paper Clip’?

If you believe all of this is ‘just a coincidence’ – go ahead and keep brushing your teeth with your ‘fluoride’ toothpaste and sucking on your sodium fluoride enhanced Coke or Pepsi product – for ignorance truly is bliss and you truly deserve what you get.

Mothers, if your little ones are having trouble concentrating at home or in school, or have been diagnosed as ‘attention deficit’ – perhaps you would be well advised to look for the culprit (and the solution to the problem) no further than your home medicine cabinet (your tube of toothpaste) and your friendly neighborhood school’s water fountain!!




Index Drugs
Prozac News


Citalopram and Luvox also contain the same fluorophenyl compound..



See also Scotchgard for same effects.



Prozac


Prozac/Paxil Facts
© 2001 - 2005 PFPC

Latest News

Notes & Observations:

Prozac is a fluorinated drug called "fluoxetine".

Paxil is a fluorinated drug called "paroxetine" (also called Seroxat, Aropax). These drugs are designed to inhibit the reuptake of serotonin (serotonin reuptake inhibitors - SSRIs) and hence interfere with the biological actions of serotonin, a neurotransmitter.

Both drugs contain fluorine and chloride. Fluoride is present as a '4-fluorophenyl' compound, part of the 'active' ingredient.

Fluorophenyl compounds are found as major metabolites in the human organism from Paxil and Prozac, as well as from pesticides as Flusilazole (Anderson et al, 1999), Fluorbenside; FOE 5043 (Christenson et al, 1996), other drugs such as dexfenfluramine ("Redux"; "Fen-Phen" - now withdrawn) (Kalin et al, 2000); Fluvastatin (Top 200 drugs) (Dain et al, 1993); Flutrimazole (skin cream) (Conte et al, 1992); AD-5423 (an anti-psychotic) (Oka et al, 1993), Bay U 3405 (Braun et al, 1990); Cisapride (also now withdrawn from US market), Leflunamide (Arava) etc...

Fluorophenyl compounds have shown to disturb thyroid hormone activity in several ways, specifically in the liver and at the hypothalamus-pituitary-thyroid (HPT) axis.

Observations: Thyroid Hormones

In depressed patients receiving paroxetine the T4 level was reduced by 11. 2% (Konig et al, 2000).

In animals chronic administration of fluoxetine resulted in a decrease in both T4 and T3 levels. The authors reported that the major effect of the drug “seems to be stimulation of TSH synthesis and release via the inhibition of T4-mediated thyroid-pituitary feedback” (Golstein et al, 1983).

In rat brain, fluoxetine has also been shown to interfere with local T3 metabolism (Eravci et al, 2000; Baumgartner et al, 1994).

Liver

In the 1930s is was first observed that all fluoride compounds, organic and inorganic ones, inhibit thyroid hormones. Prof. Kurt Kraft exposed tadpoles (bufo vulgaris, rana temporaria) to fluoride compounds including sodium fluoride, fluorotyrosine and fluorobenzoic acid (Kraft, 1937). Litzka’s experiments (1937) showed that the thyroid inhibition was due to activity in the liver (similar to PTU). Numerous fluoride compounds were used subsequently as the first line of treatment for hyperthyroidism in various countries, for several decades.

1940s experiments on animals were conducted by Euler et al. which showed that all fluoride compounds acted upon liver glycogen, the difference being a matter of amplitude (Euler et al, 1949). Some organic compounds caused identical effects in bone and teeth as inorganic fluorides (Euler et al, 1942).

In 1996, Christensen et al. tested the experimental herbicide FOE 5043 (4-fluorophenyl-containing) specifically on thyroid hormone function in the liver, after earlier tests had suggested that the observed reduced circulating serum T4 levels were due to extrathyroidal activity.

"In the liver, the actvity of hepatitic uridine glucoronosyl transferase, a major pathway of thyroid hormone biotransformation in the rat, increased in a statistically significant and dose-dependent manner, conversely hepatitic 5-monodeiodinase [D1] trended downward with dose. Bile flow and bilary excretion of T4 were increased. These data suggests that the functional status of the thyroid and pituitary glands has not been altered by treatment with FOE 5043 and that reductions in circulating levels of T4 are being mediated indirectly through an increase in the biotransformation and excretion of thyroid hormone in the liver."

Urichuk et al (1997) showed that levels of fluorophenyl metabolites after fluoxetine administration were 10-fold higher in the liver of rats than in brain.

CNS

In the 1940s numerous investigators were of the opinion that - besides being active in liver - organic fluorides could also be causing disturbances at the hypothalamus-pituitary (HP) axis, due to their high affinity for the central nervous system (CNS) (Litzka, 1937, May, 1950).

Later investigations into such compounds as fluoxetine confirmed those suspicions (Jackson et al, 1998; Baumgartner et al, 1994; Golstein et al, 1983).

In humans fluoxetine treatment reduced TRH-induced TSH release in both normal and obese women (Pijl et al, 1993). In a hypothalamic neuronal culture system fluoxetine decreased TRH levels (Jackson et al, 1998). In other tissue (rabbits - colon) it has shown to enhance TRH activity (Horita & Carino, 1982).

In humans, fluvoxamine (Luvox) also causes a decreased TSH response in the TRH test, indicating disturbances in the hypothalamus-pituitary-thyroid (HPT) axis. It caused decreased basal TSH levels (De Mendonca et al, 1997).

Fluoxetine affects both D2 and D3 deiodinase activities in the rat brain (Eravci et al, 2000; Baumgartner et al, 1994).

These deiodinases - of which there are three (D1, D2 and D3) - are responsible for T4 to T3 conversion. While D1 is mainly expressed in the liver, kidney and the thyroid, D2 is found in the central nervous system, the pituitary, skeletal muscle and adipose tissue. D3 is responsible for the production of reverse T3 (rT3).

P450 System

Fluorophenyl compounds are potent inhibitors of the cytochrome P450 (CYP) enzyme system in the liver.

Prolonged inhibition of P450 leads to thyroid hormone reduction. Thyroid hormones, in turn, modulate the levels of P450 in the liver, where the majority of thyroid hormone synthesis occurs (T4 ->T3).

Drug Interactions

Fluoxetine is a known inhibitor of multiple P450 isoenzymes, thus interfering with the metabolism of other substances (Thompson et al, 1997; 2003).

Fluoxetine thus may potentiate the effects of other drugs manyfold (Daniel et al, 1999a, 1999b). Fluoxetine potently increased (up to 13 times) the concentrations of thioridazine and its metabolites in the plasma (Daniel et al, 1999), due to synergistic pharmacodynamic effects and the influence of fluoxetine on the bioavailability of such compounds.

Selenoproteins

Studies in rat liver slices showed intracellular glutathione levels decreased and fluoride ion levels increased in a time and concentration-dependent manner by fluoxetine (Thompson et al, 1997).

Like the deiodinases, glutathione peroxidase is another selenoprotein-containing enzyme which further modulates iodine metabolism.

Glutathione peroxidase levels are considered a diagnostic tool in fluoride poisoning - discriminating between mild and severe chronic fluorosis (Guan, 1983).

Several animal studies show that fluoxetine affects T3 production in various tissue, including brain (Eravci et al, 2000; Lin et al, 1999; Baumgartner et al, 1994; Shelton et al, 1993). .

Because of their vast effects on the thyroid hormone system, it is of great importance that anybody wishing to get off such medications as Paxil, Prozac, Luvox etc. does so very gradually.

Other Assorted Prozac Facts

Infants who were breastfed by mothers taking fluoxetine demonstrated a growth curve significantly below that of infants who were breastfed by mothers who did not take the drug (Chambers et al, 1999). Newborn mouse pups exposed to paroxetine were more likely to have low birthweights (Rayburn et al, 2000). Low birth weight is related to thyroid status of the mother.

Fluoxetine has been shown to cause severe liver dysfunction such as hepatitis (Cai et al, 1999; Johnston & Wheeler, 1997; Mars et al, 1991; Friedenberg & Rothstein, 1996).

Fluoxetine has also been shown to cause secondary hyperthyroidism - originating from pituitary dysfunction (Martinez & Ortiz, 1999).

Visual hallucinations have been found associated with use of fluoxetine (Bourgeois et al, 1998).

Dyskinesia has been reported with use of fluoxetine. (Duborvski & Thomas, 1996).

Fluoxetine showed tumor-promoting activity in rat liver , as did fenfluramine, another fluorophenyl-containing fluoride compound (Lin et al, 1999). [Ed: as does PFOS - "Scotchgard")].

Like other, inorganic fluoride compounds, 4-fluorophenyl shows activity upon TXA2/PGA2 receptors (Marcin et al. 1999).

Myoclonus

“A 72-year-old woman developed rhythmic palatal movements, myoclonus, chorea, and possibly dystonia after 2 years of therapy with fluoxetine. On withdrawal of fluoxetine, the movements abated after 5 days and did not recur. A second patient, a 58-year-old man, developed myoclonic jerking and rapid, stereotypic movements of his toes after a year of fluoxetine therapy.” (Bharucha & Sethi, 1996).

REFERENCES:

Abenhaim L, Moride Y, Brenot F, Rich S et. al. - "Appetite-Suppressant Drugs and the Risk of Primary Pulmonary Hypertension" NEJM 335:609-616 (1996)

Anderson JJ, Shalaby LM, Berg DS - "Metabolism of [(14)C]flusilazole in the goat" J Agric Food Chem 47(6):2439-46 (1999)
http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Re trieve&db=PubMed&list_uids=10794648&dopt=Abstract
(Flusilazole)

Atan A, Basar MM, Aydoganli L - "Comparison of the efficacy of fluoxetine alone vs. fluoxetine plus local lidocaine ointment in the treatment of premature ejaculation" Arch Esp Urol 53(9):856-8 (2000)
http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Re trieve&db=PubMed&list_uids=11196396&dopt=Abstract

Baumgartner A, Dubeyko M, Campos-Barros A, Eravci M, Meinhold H - "Subchronic administration of fluoxetine to rats affects triiodothyronine production and deiodination in regions of the cortex and in the limbic forebrain" Brain Res 635(1-2):68-74 (1994)
http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Re trieve&db=PubMed&list_uids=8173980&dopt=Abstract

Bharucha KJ, Sethi KD - "Complex movement disorders induced by fluoxetine" Mov Disord 11(3):324-6 (1996) http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Re trieve&db=PubMed&list_uids=8723152&dopt=Abstract

Bourgeois JA, Thomas D, Johansen T, Walker DM J - “Visual hallucinations associated with fluoxetine and sertraline” Clin Psychopharmacol 18(6):482-3 (1998) http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Re trieve&db=PubMed&list_uids=9864082&dopt=Abstract.

Braun M, Schror K - "Bay U 3405 inhibits cerebral vasospasm induced by authentic thromboxane A2" Stroke 21(12 Suppl):IV152-4 (1990) http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Re trieve&db=PubMed&list_uids=2260141&dopt=Abstract

Bross R, Hoffer LJ - "Fluoxetine increases resting energy expenditure and basal body temperature in humans" Am J Clin Nutr 61(5):1020-5 (1995) http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Re trieve&db=PubMed&list_uids=7733022&dopt=Abstract

Braun M, Schror K - "Bay U 3405 inhibits cerebral vasospasm induced by authentic thromboxane A2" Stroke 21(12 Suppl):IV152-4 (1990)
http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Re trieve&db=PubMed&list_uids=2260141&dopt=Abstract
(Bay U 3405)

Chambers CD, Anderson PO, Thomas RG, Dick LM, Felix RJ, Johnson KA, Jones KL - "Weight gain in infants breastfed by mothers who take fluoxetine" Pediatrics 104(5):e61 (1999)
http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Re trieve&db=PubMed&list_uids=10545587&dopt=Abstract

Choy RK, Thomas JH - "Fluoxetine-resistant mutants in C. elegans define a novel family of transmembrane proteins" Mol Cell 4(2):143-52 (1999)
http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Re trieve&db=PubMed&list_uids=10488330&dopt=Abstract

Christenson WR, Becker BD, Wahle BS, Moore KD, Dass PD, Lake SG, Van Goethem DL, Stuart BP, Sangha GK, Thyssen JH - "Evidence of chemical stimulation of hepatic metabolism by an experimental acetanilide (FOE 5043) indirectly mediating reductions in circulating thyroid hormone levels in the male rat" Fundam Appl Toxicol 29(2):251-9 (1996)
http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Re trieve&db=PubMed&list_uids=8742323&dopt=Abstract

Cai Q, Benson MA, Talbot TJ, Devadas G, Swanson HJ, Olson JL, Kirchner JP - "Acute hepatitis due to fluoxetine therapy" Mayo Clin Proc 74(7):692-4 (1999) http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Re trieve&db=PubMed&list_uids=10405699&dopt=Abstract

Cisapride Factsheet 1:
http://www.rxlist.com/cgi/generic/cisap.htm

Conte L, Ramis J, Mis R, Forn J, Vilaro S, Reina M, Vilageliu J, Basi N - "Percutaneous absorption and skin distribution of [14C]flutrimazole in mini-pigs" Arzneimittelforschung 42(6):847-53 (1992) http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Re trieve&db=PubMed&list_uids=1418044&dopt=Abstract

Dain JG, Fu E, Gorski J, Nicoletti J, Scallen TJ - "Biotransformation of fluvastatin sodium in humans" Drug Metab Dispos 21(4):567-72 (1993) http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Re trieve&db=PubMed&list_uids=8104114&dopt=Abstract

Daniel WA, Syrek M, Wojcikowski J - "The influence of selective serotonin reuptake inhibitors on the plasma and brain pharmacokinetics of the simplest phenothiazine neuroleptic promazine in the rat" Eur Neuropsychopharmacol 9(4):337-44 (1999) http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Re trieve&db=PubMed&list_uids=10422895&dopt=Abstract

Daniel WA, Wojcikowski J - "The role of lysosomes in the cellular distribution of thioridazine and potential drug interactions" Toxicol Appl Pharmacol 158(2):115-24(1999) http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Re trieve&db=PubMed&list_uids=10406926&dopt=Abstract

De Mendonca Lima CA, Vandel S, Bonin B, Bechtel P, Carron R - "Maprotiline versus fluvoxamine: comparison of their effects on the hypothalamo-hypophyseal-thyroid axis" Encephale 23(1):48-55 (1997)
http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Re trieve&db=PubMed&list_uids=9172968&dopt=Abstract

Dihydrolenperone
http://www.google.com/search?q=cache:6usRavFBCv0:dtp ws4.ncifcrf.gov/DATA/COMPOUNDS/343513.HTML+4-fluoro phenyl&hl=en

Dubovsky SL, Thomas M - "Tardive dyskinesia associated with fluoxetine" Psychiatr Serv 47(9):991-3 (1996) http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Re trieve&db=PubMed&list_uids=8875667&dopt=Abstract

Eravci M, Pinna G, Meinhold H, Baumgartner A - "Effects of pharmacological and nonpharmacological treatments on thyroid hormone metabolism and concentrations in rat brain" Endocrinology 141(3):1027-40 (2000) FULL TEXT

Euler H, Eichler O, Hindemith H -"Über die Wirkung einiger organischer Fluoride bei chronischer Darreichung" Arch Exp. Path u Pharmakol Bd.206:75-82 (1949)

Euler H, Eichler O - "Über die Wirkung von Fluor in organischer Bindung auf das Zahnsytem der Ratte" Arch Exp Pathol Pharmakol 199:179-187 (1942)

Fluorbenside
http://www.hclrss.demon.co.uk/fluorbenside.html

Flusilazole Fact Sheet 1:
http://www.fao.org/docrep/W8053E/w8053e04.htm

Flusilazole Fact Sheet 2: Food Residues:
http://www.inchem.org/documents/jmpr/jmpmono/v95pr08. htm

Fluvastin Fact Sheet:
http://w:www.rxlist.com/cgi/generic/fluva.htm

DEXFENFLURAMINE Fen-Phen Withdrawal Notice FDA http://www.fda.gov/bbs/topics/NEWS/NEW00591.html

Friedenberg FK, Rothstein KD - "Hepatitis secondary to fluoxetine treatment" Am J Psychiatry 153(4):580(1996) http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Re trieve&db=PubMed&list_uids=8599417&dopt=Abstract

Goeringer KE, Raymon L, Christian GD, Logan BK -"Postmortem forensic toxicology of selective serotonin reuptake inhibitors: a review of pharmacology and report of 168 cases" J Forensic Sci45(3):633-48 (2000)
http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Re trieve&db=PubMed&list_uids=10855970&dopt=Abstract

Golstein J, Schreiber S, Velkeniers B, Vanhaelst L - "Effect of fluoxetine, a serotonin reuptake inhibitor, on the pituitary-thyroid axis in rat" Eur J Pharmacol 91(2-3):239-43 (1983)
http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Re trieve&db=PubMed&list_uids=6413229&dopt=Abstract

Guan ZZ - "An experimental study of blood biochemical diagnostic indices for chronic fluorosis" Zhonghua Yu Fang Yi Xue Za Zhi 25(1):33-5 (1991)
http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Re trieve&db=PubMed&list_uids=2036910&dopt=Abstract

Henry ME, Moore CM, Kaufman MJ, Michelson D, Schmidt ME, Stoddard E, Vuckevic AJ, Berreira PJ, Cohen BM, Renshaw PF - "Brain kinetics of paroxetine and fluoxetine on the third day of placebo substitution: a fluorine MRS study" Am J Psychiatry 157(9):1506-8 (2000)
http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Re trieve&db=PubMed&list_uids=10964871&dopt=Abstract

Horita A, Carino MA - “Centrally administered thyrotropin-releasing hormone (TRH) stimulates colonic transit and diarrhea production by a vagally mediated serotonergic mechanism in the rabbit” J Pharmacol Exp Ther 222(2):367-71 (1982)

Hostetter A, Ritchie JC, Stowe ZN - "Amniotic fluid and umbilical cord blood concentrations of antidepressants in three women" Biol Psychiatry 48(10):1032-4 (2000)
http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Re trieve&db=PubMed&list_uids=11082480&dopt=Abstract

Jackson IM, Luo LG - "Antidepressants inhibit the glucocorticoid stimulation of thyrotropin releasing hormone expression in cultured hypothalamic neurons" J Investig Med 46(9):470-4 (1998)
http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Re trieve&db=PubMed&list_uids=9861783&dopt=Abstract

Johnston DE, Wheeler DE - "Chronic hepatitis related to use of fluoxetine" Am J Gastroenterol 92(7):1225-6 (1997)
http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Re trieve&db=PubMed&list_uids=9219808&dopt=Abstract

Kalia M, O'Callaghan JP, Miller DB, Kramer M - "Comparative study of fluoxetine, sibutramine, sertraline and dexfenfluramine on the morphology of serotonergic nerve terminals using serotonin immunohistochemistry" Brain Res 858(1):92-105 (2000) http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Re trieve&db=PubMed&list_uids=10700602&dopt=Abstract

Konig F, Hauger B, von Hippel C, Wolfersdorf M, Kaschka WP - "Effect of paroxetine on thyroid hormone levels in severely depressed patients" Neuropsychobiology 42(3):135-8 (2000) http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Re trieve&db=PubMed&list_uids=11015031&dopt=Abstract

Kraft K - "Über die Synthese einiger aromatischer Fluorverbindungen" Knoll Research, Chem Ber. 84(2):150-156 (1951)

Kraft K - "Beiträge zur Biochemie des Fluors I.Über den Antagonismus zwischen Fluor und Thyroxin." Hoppe-Seglers Z.Physiol. Chem 245:58 -65 (1937)

Kraft K, Dengel F - "Über die Synthese einiger aromatischer Fluorverbindungen, II. Mitteilung" Chem Ber 85(6):577-582 (1952)

Lin X, Levitsky DA, King JM, Campbell TC - "The promotion effect of anorectic drugs on aflatoxin B(1)-induced hepatic preneoplastic foci" Carcinogenesis 20(9):1793-9 (1999) http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Re trieve&db=PubMed&list_uids=10469626&dopt=Abstract

Litzka G - "Die experimentellen Grundlagen der Behandlung des Morbus Basedow und der Hyperthyreose mittels Fluortyrosin" Med Wochenschr 63:1037-1040 (1937)

Marcin Róalski M, Boncler M, Wiclawska B, Watala C - "Molecular and therapeutical aspects of the blood platelet receptors antagonists" Laboratory of Haemostasis and Haemostatic Disorders, Department of Laboratory Diagnostics, Medical University, Lód , Poland
http://www.medscimonit.com/pub/vol_5/no_2/357.pdf

Mars F, Dumas de la Roque G, Goissen P - "Acute hepatitis during treatment with fluoxetine" Gastroenterol Clin Biol 15(3):270-1 (1991)
http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Re trieve&db=PubMed&list_uids=2044897&dopt=Abstract

Martinez Ortiz JJ - "Hyperthyroidism secondary to antidepressive treatment with fluoxetine" An Med Interna 16(11):583-4 (1999) http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Re trieve&db=PubMed&list_uids=10638001&dopt=Abstract

May W - "Die Basedowsche Krankheit" Aulendorf, Sandmeyer & Sohn (1950)

Meuldermans W, Hendrickx J, Lauwers W, Hurkmans R, Mostmans E, Swysen E, Bracke J, Knaeps A, Heykants J - "Excretion and biotransformation of cisapride in rats after oral administration" Drug Metab Dispos 16(3):410-9 (1988)
http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Re trieve&db=PubMed&list_uids=2900733&dopt=Abstract
(Cisapride)

Moreau X, Azorin JM, Lejeune PJ, Jeanningros R - "Red blood cell triiodothyronine uptake in unipolar major depression: effect of a chronic antidepressant treatment" Prog Neuropsychopharmacol Biol Psychiatry 24(1):23-35 (2000)

Nargund LV, Hariprasad V, Reedy GR - "Synthesis and anti-inflammatory activity of fluorinated phenyl styryl ketones and N-phenyl-5-substituted aryl-3-p-(fluorophenyl) pyrazolins and pyrazoles" J Pharm Sci 81(9):892-4 (1992) http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Re trieve&db=PubMed&list_uids=1432635&dopt=Abstract
"All compounds (0.20 mM) showed ability to denature bovine serum albumin, as observed in in vitro inhibition studies."

Ohta T, Wergedal JE, Matsuyama T, Baylink DJ, Lau KH - "Phenytoin and fluoride act in concert to stimulate bone formation and to increase bone volume in adult male rats" Calcif Tissue Int 156(5):390-7 (1995)
http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Re trieve&db=PubMed&list_uids=7621347&dopt=Abstract

Oka M, Noda Y, Ochi Y, Furukawa K, Une T, Kurumiya S, Hino K, Karasawa T - "Pharmacological profile of AD-5423, a novel antipsychotic with both potent dopamine-D2 and serotonin-S2 antagonist properties" J Pharmacol Exp Ther 264(1):158-65(1993) http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Re trieve&db=PubMed&list_uids=8093723&dopt=Abstract

Oida T, Terauchi Y, Yoshida K, Kagemoto A, Sekine Y - "Use of antisera in the isolation of human specific conjugates of haloperidol" Xenobiotica 19(7):781-93 (1989)
http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Re trieve&db=PubMed&list_uids=2773512&dopt=Abstract
(Haloperidol)

Pijl H, Koppeschaar HP, Willekens FL, Frolich M, Meinders AE - The influence of serotonergic neurotransmission on pituitary hormone release in obese and non-obese females” Acta Endocrinol (Copenh)128(4):319-24 (1993)

Prozac Data Sheet
http://www.inchem.org/documents/pims/pharm/pim651.htm

Prozac Violence:
Tracy, Ann Blake - “ The Aftermath Of Prozac, Zoloft, Luvox, Fen-Phen, & Many Other Serotonergic Drugs”
http://www.drugawareness.org/Archives/Miscellaneous/MR After.html

Rayburn WF, Gonzalez CL, Christensen HD, Kupiec TC, Jacobsen JA, Stewart JD - "Effect of antenatal exposure to paroxetine (paxil) on growth and physical maturation of mice offspring" J Matern Fetal Med 9(2):136-41 (2000)

Sarich TC, Wright JM - "Hypothyroxinemia and phenytoin toxicity: a vicious circle" Drug Metabol Drug Interact 13(2):155-60 (1996) http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Re trieve&db=PubMed&list_uids=8905247&dopt=Abstract

Schuld A, Archelos JJ, Friess E - “Visual hallucinations and psychotic symptoms during treatment with selective serotonin reuptake inhibitors: is the sigma receptor involved?” J Clin Psychopharmacol 20(5):579-80 (2000)

Shelton RC, Winn S, Ekhatore N, Loosen PT - "The effects of antidepressants on the thyroid axis in depression." Biol Psychiatry 33(2):120-6 (1993)
http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Re trieve&db=PubMed&list_uids=8439600&dopt=Abstract

Thompson DC, Perera K, London R - "Spontaneous hydrolysis of 4-trifluoromethylphenol to a quinone methide and subsequent protein alkylation" Chem Biol Interact 126(1):1-14 (2000)
http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Re trieve&db=PubMed&list_uids=10826650&dopt=Abstract

Thompson DS, Kirshner MA, Klug TL, Kastango KB, Pollock BG - “A Preliminary Study of the Effect of Fluoxetine Treatment on the 2:16-alpha-Hydroxyestrone Ratio in Young Women” Ther Drug Monit 25(1):125-8 (2003)

Urichuk LJ, Aspeslet LJ, Holt A, Silverstone PH, Coutts RT, Baker GB - “Determination of p-trifluoromethylphenol, a metabolite of fluoxetine, in tissues and body fluids using an electron-capture gas chromatographic procedure” J Chromatogr B Biomed Sci Appl 698(1-2):103-9 (1997)

Paxil Withdrawal Support Group
http://members.tripod.lycos.com/fstreicher/