Re: Digest Number 1267

[Guest guest]

Rosemary, my doc put me on 600 mgs of Caltrate to help with bone loss.

in LA AIH 99'

[Guest guest]

Kathi, I can't believe you had a biopsy done without being asleep. My doc

was so considerate to put me to sleep. I never knew anything was going on

until I woke up about 10 mins after the procedure. I was alittle sore, but

that was all.

in LA AIH 99'

[Guest guest]

..... till I got into this group I didn`t even know they would put

you to sleep for a biopsy..... didn`t even know some people had bad

experiences with them.....

I`ve had 4 and they were all quick (save one) and painless..... I was

awake and watched all of them .... I hope my next one is the same way ,

all these negative posts got me wondering...

jerry

Kathi, I can't believe you had a biopsy done without being asleep. My doc

was so considerate to put me to sleep. I never knew anything was going on

until I woke up about 10 mins after the procedure. I was alittle sore, but

that was all.

in LA AIH 99'

[Guest guest]

Joye - Who was the speaker you had at the conference? Cyndi in VA

[Guest guest]

Mooney.

cpitonyak@... wrote: Joye - Who was the speaker you had at the

conference? Cyndi in VA

[Guest guest]

My son has his five year physical, and of course I did not do the MMR, we

tested his titers and he is still immune, so no need to do this according to

Dr. G. However, Dr. G feels we should still do the polio and DPT shots, but

I am afraid to put any shots into my child. Has anyone else faced this

dilema?

Lavandowska

[Guest guest]

, we are scheduled to see Dr. G on December 10th. It is time for my 4 year

old daughter's shots. I'm afraid to do them also. Let me know what you find

out. Shona

>

> Wrom: LPTCXLYRWTQTIPWI

> Date: 2002/09/24 Tue AM 01:12:52 EDT

>

> Subject: Re: Digest Number 1267

>

>

[Guest guest]

Thanks . They are boosters. I'm just going to hold off on everything

until we see Dr. G. Her speech therapist is totally amazed at the progress that

she's made in the last 3 weeks since coming off milk products and sugar. She is

more focused and interacting so much more. Her verbal skills are improving by

leaps and bounds. Can't wait to see Dr. G to see if we can help this along

further. I haven't seen that much improvement in my 2 year old yet. Wonder

why??

>

> Wrom: LSZLKBRNVWWCUFPEGAUTFJMVRESKPNKMBIPBARHD

> Date: 2002/09/24 Tue PM 08:33:14 EDT

>

> Subject: Re: Re: Digest Number 1267

>

>

[Guest guest]

My 2 year old is much calmer than he was. I think I'm just so ready to hear

language from him that I may be jumping the gun. He is much more aware of

things and his surroundings than he was. He actually sits in my lap now and

reads a book with me. That's a first. It's so hard to figure out what triggers

he has, since he's a human garbage disposal. He eats everything you put in

front of him. I'm beginning to wonder about his sugar free cookies. They don't

contain milk, but he's beginning to want them a lot. Our appt isn't until Dec

10th and they want us to do labs out there. A note on my 4 year old. Just

yesterday her speech therapist said that we were ready to start playing games

like Candyland with her. That brought me to my knees. Two months ago we were

nowhere near being ready for that. Funny how this makes you appreciate every

little thing. Our speech therapist is ready to spread the word. She may be

coming with us to the appt. Any other suggestions about food triggers? This is

really hard to do, but the results are worth it. Thanks. Shona

>

> Wrom: YXOEAIJJPHSCRTNHGSWZIDREXCAXZOWCONEUQZAA

> Date: 2002/09/30 Mon PM 10:49:25 EDT

>

> Subject: Re: Re: Digest Number 1267

>

>

[Guest guest]

officinalis tincture and l-Lysine have helped many people get

various Herpes viruses into suppression.

mjh

> From: " mariatassios2 <mariatassios2@...> " <mariatassios2@...>

> Subject: HERPES 2 VIRUS QUERY

>

> Hi All

>

> Does any know how to get rid of the HERPES 2 VIRUS which has

> mutated in the system.

>

> Are there any products on the market that can help?

>

> Look forward to some information.

>

> MARIA

>

[Guest guest]

Re: the articla below. What protocols would cause

dopamine to increase or decrease?

Thanks,

Jane

Dopamine link to psychiatric and neurological

disorders

Medical Research News

Published: Sunday, 23-Oct-2005

A gene that regulates dopamine levels in the brain is

involved in the

development of schizophrenia in children at high risk

for the disorder,

say

researchers at the Stanford University School of

Medicine, Lucile

Packard

Children's Hospital and the University of Geneva.

The finding adds to mounting evidence of dopamine's

link to psychiatric

and

neurological disorders. It may also allow physicians

to pinpoint a

subset of

these children for treatment before symptoms start.

" The hope is that we will one day be able to identify

the highest-risk

groups and intervene early to prevent a lifetime of

problems and

suffering, "

said Allan L. Reiss, MD. " As we gain a much better

understanding of

these

disorders, we can design treatments that are much more

specific and

effective. "

Reiss is the Robbins Professor of Psychiatry and

Behavioral Sciences at

Stanford and director of the school's Center for

Interdisciplinary

Brain

Sciences Research. He is also a child and adolescent

psychiatrist at

Packard

Children's Hospital at Stanford. The research, which

will be published

online Oct. 23, will appear in print in the November

issue of Nature

Neuroscience.

Dopamine levels have been implicated in many

neurological conditions,

including Parkinson's disease and psychosis. Data from

this and other

studies suggest a kind of Goldilocks effect for this

important chemical

messenger: too little or too much can dramatically

interfere with

normal

cognition, behavior and motor skills. Nudging these

levels back into

the

" just-right " range may help treat or cure some

conditions.

Schizophrenia is a brain disease that affects about 1

percent of people

in

this country and can manifest itself through

agitation, catatonia and

psychosis. Although the disorder sometimes runs in

families, it can

also

occur spontaneously. Scientists have suspected for

many years that

dopamine

was involved, due in part to the success of older

psychiatric drugs

that

function by interacting with dopamine receptors in the

brain. But the

root

cause of schizophrenia has remained elusive.

Reiss and the study's first author Doron Gothelf, MD,

a child

psychiatrist

and postdoctoral scholar at Stanford, studied 24

children with a small

deletion in one copy of chromosome 22. About 30

percent of children

with

this deletion, which occurs in about one in 4,000

births, will develop

schizophrenia or a related psychotic disorder. These

children also

often

have special facial features, cardiac defects and

cleft anomalies that

often

make their speech hypernasal. Although these

characteristics make it

possible to identify them before psychiatric disorders

develop, the

disorder, called velocardiofacial syndrome, is

under-diagnosed and

under-recognized in this country despite its link to

schizophrenia.

" We have strong evidence that this deletion is a major

risk factor for

the

development of schizophrenia or related psychotic

disorders, " said

Reiss.

" We asked, 'What is it about this deletion that causes

such an increase

in

risk?' "

The answer lay in the fact that one of the missing

genes encodes a

dopamine-degrading protein called COMT. Natural

variations in the gene

generate two versions of the protein: one with high

activity, one with

low.

Because most people have two copies of the gene, it

doesn't usually

matter

which versions of COMT they inherit; high-high,

high-low and low-low

all

seem to provide enough COMT activity to get the job

done (though some

combinations confer a mild advantage for some

cognitive tasks).

But children with the deletion have only the one copy

that remains on

their

intact chromosome 22. Reiss and Gothelf, who is also

an assistant

professor

at Tel Aviv University in Israel, surmised that a

single copy of the

low-activity COMT might not dispose of enough dopamine

to produce

optimal

brain function. They set out to determine if the

clinical course of the

children with deletions who developed schizophrenia

varied with the

version

of the COMT protein they had.

The researchers matched the age, gender, ethnicity and

IQ of the 24

children

with the deletion with 23 children with developmental

disabilities of

unknown causes. They then tested their subjects'

verbal IQ and

cognitive

abilities. None of the children in either group had

yet experienced any

psychotic symptoms. They also measured the size of the

children's

prefrontal

cortex - an area of the brain where COMT activity is

particularly

important

and that is strongly associated with schizophrenia.

They repeated the

same

tests after about five years, when their subjects

reached late

adolescence

or early adulthood.

As expected, about 29 percent, or seven, of the

children with the

deletion

had developed a psychotic disorder by the second round

of testing,

compared

with only one child in the control group. Of these

seven, those with

the

low-activity version of COMT had experienced a

significantly greater

drop in

their verbal IQ and expressive language skills and a

markedly greater

decrease in the volume of their prefrontal cortex than

did their peers

with

the more highly active version of COMT. The psychotic

symptoms of the

low-activity subset were also significantly more

severe.

In contrast, members of the control group experienced

no significant

differences in any of these categories, regardless of

their COMT

profiles.

" What's interesting about this finding is that the

disease course in

the

individuals with low-activity COMT looked remarkably

like idiopathic

schizophrenia, " said Reiss, who hopes to use this and

future data to

develop

a model for other causes of schizophrenia.

" Although this deletion probably causes less than 5

percent of

schizophrenia

cases, it's the only well-defined genetic risk factor

we have right

now, "

said Reiss. " In the future, researchers will likely

discover multiple

causes

of this disorder, with complex interactions between

genetic and

environmental risk factors. But COMT activity appears

to be an

important

contributory factor for the development of psychosis

in the chromosome

22

deletion syndrome. "

The researchers next plan to extend their studies to

younger children,

and

to repeat the above study using multiple time points

to more precisely

catch

the ongoing development of the disorder.

http://www.med.stanford.edu/

__________________________________

FareChase: Search multiple travel sites in one click.

http://farechase.

[Guest guest]

Jane,

It is my understanding that excess dopamine can cause paranoia -- a common

feature of schizophrenia. Interestingly, caffiene, nicotine, exercise and

cocaine also increase dopamine in the brain. If a person is placed on

wellbutrin, and drinks a lot of coffee, smokes and does a lot of exercise --

they can demonstrate schizophregnic behaviors. Person using cocaine, of course,

can exhibit drug induced schizophrenia. It is an interesting process.

It is my understanding that increasing Alpha in the occiptal sites increases

dopamine. I believe to be in balance, a person's brain should be producing more

alpha on the left (O1) than the right (O2). I would welcome hearing more

information from others on the list serve!

--

Warmly,

This email and any attachments may contain confidential information and it is

intended for the addressee only. If you are not the intended recipient, you

should destroy this message and notify the sender by reply email. If you are

not the addressee, any disclosure, reproduction or transmission of this email is

strictly prohibited.

>

> Re: the articla below. What protocols would cause

> dopamine to increase or decrease?

>

> Thanks,

> Jane

>

> Dopamine link to psychiatric and neurological

> disorders

> Medical Research News

> Published: Sunday, 23-Oct-2005

>

>

>

> A gene that regulates dopamine levels in the brain is

> involved in the

> development of schizophrenia in children at high risk

> for the disorder,

> say

> researchers at the Stanford University School of

> Medicine, Lucile

> Packard

> Children's Hospital and the University of Geneva.

> The finding adds to mounting evidence of dopamine's

> link to psychiatric

> and

> neurological disorders. It may also allow physicians

> to pinpoint a

> subset of

> these children for treatment before symptoms start.

>

> " The hope is that we will one day be able to identify

> the highest-risk

> groups and intervene early to prevent a lifetime of

> problems and

> suffering, "

> said Allan L. Reiss, MD. " As we gain a much better

> understanding of

> these

> disorders, we can design treatments that are much more

> specific and

> effective. "

>

> Reiss is the Robbins Professor of Psychiatry and

> Behavioral Sciences at

> Stanford and director of the school's Center for

> Interdisciplinary

> Brain

> Sciences Research. He is also a child and adolescent

> psychiatrist at

> Packard

> Children's Hospital at Stanford. The research, which

> will be published

> online Oct. 23, will appear in print in the November

> issue of Nature

> Neuroscience.

>

> Dopamine levels have been implicated in many

> neurological conditions,

> including Parkinson's disease and psychosis. Data from

> this and other

> studies suggest a kind of Goldilocks effect for this

> important chemical

> messenger: too little or too much can dramatically

> interfere with

> normal

> cognition, behavior and motor skills. Nudging these

> levels back into

> the

> " just-right " range may help treat or cure some

> conditions.

>

> Schizophrenia is a brain disease that affects about 1

> percent of people

> in

> this country and can manifest itself through

> agitation, catatonia and

> psychosis. Although the disorder sometimes runs in

> families, it can

> also

> occur spontaneously. Scientists have suspected for

> many years that

> dopamine

> was involved, due in part to the success of older

> psychiatric drugs

> that

> function by interacting with dopamine receptors in the

> brain. But the

> root

> cause of schizophrenia has remained elusive.

>

> Reiss and the study's first author Doron Gothelf, MD,

> a child

> psychiatrist

> and postdoctoral scholar at Stanford, studied 24

> children with a small

> deletion in one copy of chromosome 22. About 30

> percent of children

> with

> this deletion, which occurs in about one in 4,000

> births, will develop

> schizophrenia or a related psychotic disorder. These

> children also

> often

> have special facial features, cardiac defects and

> cleft anomalies that

> often

> make their speech hypernasal. Although these

> characteristics make it

> possible to identify them before psychiatric disorders

> develop, the

> disorder, called velocardiofacial syndrome, is

> under-diagnosed and

> under-recognized in this country despite its link to

> schizophrenia.

>

> " We have strong evidence that this deletion is a major

> risk factor for

> the

> development of schizophrenia or related psychotic

> disorders, " said

> Reiss.

> " We asked, 'What is it about this deletion that causes

> such an increase

> in

> risk?' "

>

> The answer lay in the fact that one of the missing

> genes encodes a

> dopamine-degrading protein called COMT. Natural

> variations in the gene

> generate two versions of the protein: one with high

> activity, one with

> low.

>

> Because most people have two copies of the gene, it

> doesn't usually

> matter

> which versions of COMT they inherit; high-high,

> high-low and low-low

> all

> seem to provide enough COMT activity to get the job

> done (though some

> combinations confer a mild advantage for some

> cognitive tasks).

>

> But children with the deletion have only the one copy

> that remains on

> their

> intact chromosome 22. Reiss and Gothelf, who is also

> an assistant

> professor

> at Tel Aviv University in Israel, surmised that a

> single copy of the

> low-activity COMT might not dispose of enough dopamine

> to produce

> optimal

> brain function. They set out to determine if the

> clinical course of the

> children with deletions who developed schizophrenia

> varied with the

> version

> of the COMT protein they had.

>

> The researchers matched the age, gender, ethnicity and

> IQ of the 24

> children

> with the deletion with 23 children with developmental

> disabilities of

> unknown causes. They then tested their subjects'

> verbal IQ and

> cognitive

> abilities. None of the children in either group had

> yet experienced any

> psychotic symptoms. They also measured the size of the

> children's

> prefrontal

> cortex - an area of the brain where COMT activity is

> particularly

> important

> and that is strongly associated with schizophrenia.

> They repeated the

> same

> tests after about five years, when their subjects

> reached late

> adolescence

> or early adulthood.

>

> As expected, about 29 percent, or seven, of the

> children with the

> deletion

> had developed a psychotic disorder by the second round

> of testing,

> compared

> with only one child in the control group. Of these

> seven, those with

> the

> low-activity version of COMT had experienced a

> significantly greater

> drop in

> their verbal IQ and expressive language skills and a

> markedly greater

> decrease in the volume of their prefrontal cortex than

> did their peers

> with

> the more highly active version of COMT. The psychotic

> symptoms of the

> low-activity subset were also significantly more

> severe.

>

> In contrast, members of the control group experienced

> no significant

> differences in any of these categories, regardless of

> their COMT

> profiles.

>

> " What's interesting about this finding is that the

> disease course in

> the

> individuals with low-activity COMT looked remarkably

> like idiopathic

> schizophrenia, " said Reiss, who hopes to use this and

> future data to

> develop

> a model for other causes of schizophrenia.

>

> " Although this deletion probably causes less than 5

> percent of

> schizophrenia

> cases, it's the only well-defined genetic risk factor

> we have right

> now, "

> said Reiss. " In the future, researchers will likely

> discover multiple

> causes

> of this disorder, with complex interactions between

> genetic and

> environmental risk factors. But COMT activity appears

> to be an

> important

> contributory factor for the development of psychosis

> in the chromosome

> 22

> deletion syndrome. "

>

> The researchers next plan to extend their studies to

> younger children,

> and

> to repeat the above study using multiple time points

> to more precisely

> catch

> the ongoing development of the disorder.

>

> http://www.med.stanford.edu/

>

>

>

> __________________________________

> FareChase: Search multiple travel sites in one click.

> http://farechase.

>

>

>

>

>

[Guest guest]

And a good two sense it is. Quality of life is a very important

part of survivalship!!!!

With warm regards,

Matt

ville, FL

DX January 2005

Gleevec March 2005

Tasigna November 2008

In a message dated 2/19/2008 12:00:51 P.M. Eastern Standard Time,

kttweety@... writes:

Hey Group. . .

I have said this before and I will say it again. . .

" We are a Statistic to the Hematologist/ " We are a Statistic to the

Hematologist/<WBR>Oncologist; but each one of us is an Individual in our

Survival and

the choice(s) we make on our treatment is the most importan

Due to 'side effects', I was unable to tolerate 400 or 600 m.g. of our gold

on a daily basis; therefore, my daily dosage was 300 m.g. After reaching

0.00136 in 1/2005; I began to 'pulse'.

My reasoning was 'if it took 300 m.g. to reach '0'; I didn't need that

dosage daily to maintain my response'. My RT-PCR Test was 0.00021 on February

13th

and I take 300 m.g.~~3 - 4 days a week and my side effects are greatly

diminished from the H**L I went through after diagnosis.

" I am not a Doctor, never portrayed one on TV; nor do I aspire to be a

Physician in another life " . This is FYI~~my 2 cents only.

Take care, as always I have ALL in my prayers. . . " K "

" K "

" I AIN'T FINISHED YET " !!!

[Non-text portions of this message have been removed]

**************Ideas to please picky eaters. Watch video on AOL Living.

(http://living.aol.com/video/how-to-please-your-picky-eater/rachel-campos-duffy/

2050827?NCID=aolcmp00300000002598)

[Guest guest]

Hey Group. . .

I have said this before and I will say it again. . .

" We are a Statistic to the Hematologist/Oncologist; but each one of us is an

Individual in our Survival and the choice(s) we make on our treatment is the

most important decision we will make during our lifetime " .

Due to 'side effects', I was unable to tolerate 400 or 600 m.g. of our gold on

a daily basis; therefore, my daily dosage was 300 m.g. After reaching 0.00136 in

1/2005; I began to 'pulse'.

My reasoning was 'if it took 300 m.g. to reach '0'; I didn't need that dosage

daily to maintain my response'. My RT-PCR Test was 0.00021 on February 13th and

I take 300 m.g.~~3 - 4 days a week and my side effects are greatly diminished

from the H**L I went through after diagnosis.

" I am not a Doctor, never portrayed one on TV; nor do I aspire to be a

Physician in another life " . This is FYI~~my 2 cents only.

Take care, as always I have ALL in my prayers. . . " K "

" K "

" I AIN'T FINISHED YET " !!!

[Guest guest]

I totally agree... I think your cents are worth so much more... By

pure necessity sometimes we 'figure' things out! Just imagine if

everyone were put on those much smaller doses... GET me a

calculator.. that wouldn't be in the drug company's best interest I

suspect. Just a thought... maybe I'm way off base. I have " self

adjusted " my doses of Sprycel..unfortunately... had great difficulty

finding decent care etc. and had horrible side effects. STill early.

Trying to get into CML guru eventually (no ins).

>

> Hey Group. . .

> I have said this before and I will say it again. . .

> " We are a Statistic to the Hematologist/Oncologist; but each one

of us is an Individual in our Survival and the choice(s) we make on

our treatment is the most important decision we will make during our

lifetime " .

> Due to 'side effects', I was unable to tolerate 400 or 600 m.g.

of our gold on a daily basis; therefore, my daily dosage was 300 m.g.

After reaching 0.00136 in 1/2005; I began to 'pulse'.

> My reasoning was 'if it took 300 m.g. to reach '0'; I didn't need

that dosage daily to maintain my response'. My RT-PCR Test was

0.00021 on February 13th and I take 300 m.g.~~3 - 4 days a week and

my side effects are greatly diminished from the H**L I went through

after diagnosis.

> " I am not a Doctor, never portrayed one on TV; nor do I aspire to

be a Physician in another life " . This is FYI~~my 2 cents only.

> Take care, as always I have ALL in my prayers. . . " K "

>

>

>

> " K "

> " I AIN'T FINISHED YET " !!!

>

>

>

>

[Guest guest]

Ref Antidepressants/SSRIs

Given my experience with my Hashimotos Husband

I would caution any Thyroid patient to reconsider taking these

They are hell to get on and even more hell to get off and they are not nessecary

If the doctors properly treat the Hypothyroidism with the correct replacement thyroid medication and the correct dosage theres no need for anti depressants

In most cases Thyroxine is the real cause of many many symptoms especially pain and depression /anxiety

IIf you can switch to Armour you should find life a lot easier and worth living

Pat

[Guest guest]

Now - there's the voice of reason. I am with this 100%.

Luv - Sheila

Ref Antidepressants/SSRIs

Given my experience with my Hashimotos Husband

I would caution any Thyroid patient to reconsider taking

these

They are hell to get on and even more hell to get off

and they are not nessecary

If the doctors properly treat the Hypothyroidism with

the correct replacement thyroid medication and the correct dosage theres no

need for anti depressants

In most cases Thyroxine is the real cause of many many

symptoms especially pain and depression /anxiety

IIf you can switch to Armour you should find life a lot

easier and worth living

Pat

 

[Guest guest]

I was given AD's before I was even diagnosed with Hashis, are you saying thyroxine causes depression and anxiety, if you that is worrying for many of us taking it, and for those of us already feeling vunerable dont need to hear that about thyroxine when its meant to be helping us

Ref Antidepressants/ SSRIs

Given my experience with my Hashimotos Husband

I would caution any Thyroid patient to reconsider taking these

They are hell to get on and even more hell to get off and they are not nessecary

Pat

[Guest guest]

Many

sufferers of hypothyroidism have clinical depression caused through the fact their

brain is not getting the thyroid hormone it needs - and the sad thing is that

for a  large minority of these, levothyroxine is insufficient to lift that

depression - in fact, is insufficient for a lot of bodily functions. For those

who cannot convert T4 to T3, levothyroxine is the worst medication anybody

could take - and we have Thyroid Associations who are happy to recommend this

one and only medication to every person in the world and not  the reason WHY

their patients remain ill and depressed. This is why doctors keep peddling

their antidepressants - which mask the true cause of their depression - only

causing further problems down the line.  Many people taking T4 alone appear to

be doing OK, but for those who have many different symptoms, they need a

medication containing T3 - either synthetic or natural.

Sheila

I was given AD's before

I was even diagnosed with Hashis, are you saying thyroxine causes depression

and anxiety, if you that is worrying for many of us taking it, and for those

of us already feeling vunerable dont need to hear that about thyroxine when its

meant to be helping us

Ref Antidepressants/ SSRIs

Given my experience with my Hashimotos Husband

I would caution any Thyroid patient to

reconsider taking these

They are hell to get on and even more hell to

get off and they are not nessecary

Pat

[Guest guest]

I just hope I am one of those people who convert ok, but I am still not optimum yet on thyroxine and I think thats why my depression and anxiety reared its head again when I stopped for 3 weeks

Many sufferers of hypothyroidism have clinical depression caused through the fact their brain is not getting the thyroid hormone it needs - and the sad thing is that for a large minority of these, levothyroxine is insufficient to lift that depression - in fact, is insufficient for a lot of bodily functions. For those who cannot convert T4 to T3, levothyroxine is the worst medication anybody could take - and we have Thyroid Associations who are happy to recommend this one and only medication to every person in the world and not the reason WHY their patients remain ill and depressed. This is why doctors keep peddling their antidepressants - which mask the true cause of their depression - only causing further problems down the line. Many people taking T4 alone appear to be doing OK, but for those who have many different symptoms, they

need a medication containing T3 - either synthetic or natural.

Sheila

I was given AD's before I was even diagnosed with Hashis, are you saying thyroxine causes depression and anxiety, if you that is worrying for many of us taking it, and for those of us already feeling vunerable dont need to hear that about thyroxine when its meant to be helping us

Ref Antidepressants/ SSRIs

Given my experience with my Hashimotos Husband

I would caution any Thyroid patient to reconsider taking these

They are hell to get on and even more hell to get off and they are not nessecary

Pat

[Guest guest]

Hi

There is no reason whatsoever why thyroxine would cause depression

and anxiety, its a replacement hormone.

Chris

>

> I was given AD's before I was even diagnosed with Hashis, are you

saying thyroxine causes depression and anxiety, if you that is

worrying for many of us taking it, and for those of us already

feeling vunerable dont need to hear that about thyroxine when its

meant to be helping us

>

>

>

>

>

>

>

>

>

>

>

>

>

>

>

>

>

>

>

>

>

>

>

> Ref  Antidepressants/ SSRIs

>  

> Given my experience with my Hashimotos Husband

> I would caution any Thyroid patient to reconsider taking these

>  

> They are hell to get on and even more hell to get off and they are

not nessecary

>  

>  

> Pat

>

[Guest guest]

Hi Chris

Yes I thought that too, the symptoms of low thyroid cause anxiety and depression and thyroxine is given to correct that, thanks. The only way I think it could cause anxiety is if the dose is too high and you become hyper

Hi There is no reason whatsoever why thyroxine would cause depression and anxiety, its a replacement hormone.Chris>> I was given AD's before I was even diagnosed with Hashis, are you saying thyroxine causes depression and anxiety, if you that is worrying for many of us taking it, and for those of us already feeling vunerable dont need to hear that about thyroxine when its meant to be helping us> > > > > > > > > > > > > > > > > > > > > > > > Ref Antidepressants/ SSRIs>  > Given my experience with my Hashimotos

Husband > I would caution any Thyroid patient to reconsider taking these > Â > They are hell to get on and even more hell to get off and they are not nessecary > Â > Â > Pat>

[Guest guest]

Not if you need T3 Chris. We should

replace the hormone we are not making and for those who are unable to convert

T4 to T3, they need T3 in some form. I am not saying is unable to

convert, but she needs to get her dose of levothyroxine increased as she is not

getting back her health on 50 mcgs T4. If people are not converting when taking

thyroxine only, this could be a cause of clinical depression.

Sheila

There is no reason whatsoever why thyroxine would cause depression

and anxiety, its a replacement hormone.

Chris

[Guest guest]

I have just recently upped to 75mcg over the last few days, had only been on 50 for 2 weeks and then before that 25/50 alternate days for 3 weeks, so I think I can do this last increase safely, I have only had 2 T3 tests done and it was low but within range so hopefully with the added HC the next test might show an improvement

From: Sheila <sheilaturner@...>Subject: RE: Re: Digest Number 1267thyroid treatment Date: Friday, 21 November, 2008, 9:37 AM

Not if you need T3 Chris. We should replace the hormone we are not making and for those who are unable to convert T4 to T3, they need T3 in some form. I am not saying is unable to convert, but she needs to get her dose of levothyroxine increased as she is not getting back her health on 50 mcgs T4. If people are not converting when taking thyroxine only, this could be a cause of clinical depression.

SheilaThere is no reason whatsoever why thyroxine would cause depression and anxiety, its a replacement hormone.Chris

[Guest guest]

This was sent to me privately so am forwarding it to the group

From: nambucca@... <nambucca@...>Subject: Re: Fw: Re: Digest Number 1267xxsarahxx_40@...Cc: thyroidpatientadvicacy@...Date: Friday, 21 November, 2008, 4:20 PM

Thyroxine is not a true replacement hormone

Its a copy hormone made from petroleum products and since its only T4 its inadequate to deal with the mass of hormones that a normal brain needs to function correctly

Anyone who is unable to tolerate Thyroxine or for that matter T3 because they are also chemically allergic will indeed find that Thyroxine causes depression and a host of other problems especially diverse muscle and joint pains