Your SSRi is interfering with your Thyroid!! As well as killing adrenals

[Guest guest]

Oh my goodness, it all ties in! The way these drugs suck out all the

adrenal glands too which would increase the cortisol thus making

someone for a short time feel slightly better because they will be

utilizing the T3 better in the cells from the increased output but

then as here explains

http://www.antidepressantsfacts.com/pinealstory.htm how they work by

increasing the output of the adrenals until exhaustion!

Here is an extract from …

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.

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 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)

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