Fwd: [SSRI-Research] Serious indictment of our latest wonder drugs

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[sSRI-Research] Serious indictment of our latest " wonder drugs "

 

Preventive Psychiatry E-Newsletter # 60

 

Prozac/Paxil Facts

© 2001 - 2003 PFPC

 

Latest News:

 

June 19th, 2003: FDA to review reports of a possible increased risk of

suicidal thinking and suicide attempts in children and adolescents under the

age of 18 treated with Paxil. Reports of studies showing that Paxil is no

more effective than placebo in children.

 

June 10, 2003: UK Department of Health recommends that Paxil (Seroxat in

Europe) should not be used in children under the age of 18 due to safety

concerns of increased self-harm in children taking that medication.

 

===================

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other drugs such as dexfenfluramine ( " Redux " ; " Fen-Phen " - now withdrawn)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withdrawn from US market), Leflunamide (Arava) etc...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

 

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).

 

Liver

 

In the 1930s it 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.

 

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 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).

 

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 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).

 

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).

 

 

 

 

 

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