Prozac is 94% fluoride!http://www.antidepressantsfacts.com/2003-08-Prozac-Paxil-Fluorophenyl.htm
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1999), Fluorbenside; FOE 5043 (Christenson et al, 1996), other drugs such as dexfenfluramine ("Redux"; "Fen-Phen" - now withdrawn) (Kalin et al, 2000); Fluvastatin (Top 200 drugs) (Dain et al, 1993); Flutrimazole (skin cream) (Conte et al, 1992); AD-5423 (an anti-psychotic) (Oka et al, 1993), Bay U 3405 (Braun et al, 1990); Cisapride (also now withdrawn from US market), Leflunamide (Arava) etc...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.
In depressed patients receiving paroxetine the T4 level was reduced by 11. 2% (Konig et al, 2000).
In animals chronic administration of fluoxetine results 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).
In the 1930s is was first observed that all fluoride compounds, organic and inorganic ones, inhibit thyroid hormones. This was first established in the 1930s by experiments conducted by Prof. Kurt Kraft who exposed tadpoles (bufo vulgaris, rana temporaria) to fluoride compounds including sodium fluoride, fluorotyrosine and fluorobenzoic acid (Kraft, 1937). 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.
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 has been found to inhibit 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).
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).
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.
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 causes a decline in T3 levels and 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).
Massive list of references at link!!! Alex was saying that they add Prozac to water with Fluoride. That means that they found the processed compound fluoxetine alongside with fluoride...but, they both do the same thing.