Re: Question for Rich, and some random thoughts

[Guest guest]

Hi Jill,

Thought I add my 2cents worth:

I have not added any Metal RNAs or Immune Factors(IMFs) yet. I am just still

supporting the Methylation cycle nicely(I think).

I am taking a little break before I dive into the more heavy part of Step 2. I

am only doing the beginning of Step 2(4 months) and supporting the Mitochondria.

It still amazing how I am still dumping metals especially the Mercury.

I believe the Urine Toxic Metals runs $110. and the Urine toxic Metals &

Essentials is $190. from www.testing4health.com. I average my testing every 3

to 4 weeks alternating the 2 tests. Yes . . . it is expensive. I had to cancel

my order for my GAR after six months because of the expense. I am a little

dissapointed because it would have been a Extended(personalized) GAR where she

looks at all the records s you send her instead of just the Genetics. I sent her

at least one hundred pages. The Extended GAR is no longer available because she

does not have the time. I hope I won't be sorry someday. I figure I can try and

study enough to do my own GAR with all the books, DVD's, this group and the

forum.

Best wishes,

Sue T

jill1313 <jenbooks13@...> wrote:

Rich, this question, I could answer for myself if I go back and read

all the posts of yours I've printed out, and/or googled some pathways,

but I thought I'd just ask it anyway.

The ACE deletion--which it turns out I have, Sara probably has, Janet

has, Sue has...is this in everybody who has taken the Yasko test? If

so, does this somehow fit in with your high cortisol idea? Because if

the ACE deletion renders one even more vulnerable to the stress

response, wouldn't that mean one might have excessively elevated

cortisol for longer? And couldn't one really crash into fatigue?

Could the ACE deletion be a key to cfids?

Also, , in terms of excreting metals on one's own, I see from

Amy's supplement DVD (which I'm now watching) and from the 2006 DVD's,

that she suggests the (very expensive) charting every week or two with

urine spot tests. Apparently you fix the methylation cycle, see a peak

in metals excretion and a return to baseline, and at that point add in

more 'aggressive' approaches to detox more metals. I assume this is

what Sue is doing. Anyway, to follow the whole program in an ideal

mode would be really quite expensive. I guess one (i.e. me) has to

really pick and choose the supplements. I doubt I can be doing spot

urines every week. I think they are $55 each? That's what my holistic

doc remembered.

I do think I'm going to have to spring for one OATS and one urine

amino acid test. The latter will tell me how to approach taurine.

[Guest guest]

Hi, Jill.

Out of nine PWCs for whom I now have these data, eight are

homozygous for ACE (deletion 16), and one is homozygous for ACE

(inclusion 16).

The ACE deletion SNP would tend to raise the secretion of

aldosterone by the adrenals, but I don't think it would affect

cortisol secretion. However, it raises the level of angiotensisn

II, and there is evidence that angiotensin II increases the

production of oxidizing free radicals. See abstract below. So

maybe its role in biasing a person toward developing CFS is that it

stacks one more straw on the camel's back in the direction of

producing oxidative stress, and thus depleting glutathione, just as

I suspect the CYP1B1 SNP does in women, in detoxing estradiol.

More and more, based on what I'm seeing, my motto is

becoming, " Follow the glutathione. "

Rich

>

> Rich, this question, I could answer for myself if I go back and

read

> all the posts of yours I've printed out, and/or googled some

pathways,

> but I thought I'd just ask it anyway.

>

> The ACE deletion--which it turns out I have, Sara probably has,

Janet

> has, Sue has...is this in everybody who has taken the Yasko test?

If

> so, does this somehow fit in with your high cortisol idea? Because

if

> the ACE deletion renders one even more vulnerable to the stress

> response, wouldn't that mean one might have excessively elevated

> cortisol for longer? And couldn't one really crash into fatigue?

>

> Could the ACE deletion be a key to cfids?

>

> Also, , in terms of excreting metals on one's own, I see from

> Amy's supplement DVD (which I'm now watching) and from the 2006

DVD's,

> that she suggests the (very expensive) charting every week or two

with

> urine spot tests. Apparently you fix the methylation cycle, see a

peak

> in metals excretion and a return to baseline, and at that point

add in

> more 'aggressive' approaches to detox more metals. I assume this is

> what Sue is doing. Anyway, to follow the whole program in an ideal

> mode would be really quite expensive. I guess one (i.e. me) has to

> really pick and choose the supplements. I doubt I can be doing spot

> urines every week. I think they are $55 each? That's what my

holistic

> doc remembered.

>

> I do think I'm going to have to spring for one OATS and one urine

> amino acid test. The latter will tell me how to approach taurine.

>

[Guest guest]

Hi, Jill.

Sorry, I forgot to paste the abstract into my previous post. Here

it is.

Rich

Curr Hypertens Rep. 2000 Apr;2(2):167-73.

Free radical production and angiotensin.

Wolf G.

University of Hamburg, University Hospital Eppendorf, Department of

Medicine, Division of Nephrology and Osteology, Pavilion 61,

istrasse 52, D-20246 Hamburg, Germany. WOLF@...

Angiotensin II (ANG II) has multiple effects on cardiovascular and

renal cells, including vasoconstriction, cell growth, induction of

proinflammatory cytokines, and profibrogenic actions. Recent studies

provide evidence that ANG II could stimulate intracellular formation

of reactive oxygen species (ROS) such as the superoxide anion (O2-).

This ANG II-mediated ROS formation exhibits different kinetic and

lower absolute concentrations than those traditionally observed

during the respiratory burst of phagocytic cells, but it likely

involves similar membrane-bound NAD(P)H-oxidases. Current evidence

suggests that ANG II, through AT1-receptor activation, upregulates

several subunits of this multienzyme complex, resulting in an

increase in intracellular O2- concentration. ROS are involved in

several signal pathways, and redox-sensitive transcriptional factors

(AP-1, NF-kappaB) have been characterized. ANG II-induced ROS play a

pivotal role in several pathophysiologic situations of vascular and

renal cells such as hypertension, endothelial dysfunction, nitrate

tolerance, atherosclerosis, and cellular remodeling. Although these

perceptions suggest that drugs interfering with ANG II effects (ACE

inhibitors, AT1 -receptor antagonist) may serve as antioxidants,

preventing vascular and renal changes, the clinical studies are not

so straightforward. In fact, only specific risk groups, such as

patients with diabetes mellitus or renal insufficiency, may benefit

from ACE inhibitors, whereas hard endpoints showed no advantage for

ACE inhibitors in patients with essential hypertension.

PMID: 10981145 [PubMed - indexed for MEDLINE]

[Guest guest]

Thanx Sue that is much appreciated. When I am ready to start Step 1 I

may backchannel you. I did not realize there used to be an extended

GAR available. I do think one could ask questions on site--or research

on site and get some help? Its unfortunate she no longer has time for

that. I wish there were someone extremely smart, the equivalent of a

grad student in a doctoral program, whom she could train.

> Rich, this question, I could answer for myself if I go

back and read

> all the posts of yours I've printed out, and/or googled some pathways,

> but I thought I'd just ask it anyway.

>

> The ACE deletion--which it turns out I have, Sara probably has, Janet

> has, Sue has...is this in everybody who has taken the Yasko test? If

> so, does this somehow fit in with your high cortisol idea? Because if

> the ACE deletion renders one even more vulnerable to the stress

> response, wouldn't that mean one might have excessively elevated

> cortisol for longer? And couldn't one really crash into fatigue?

>

> Could the ACE deletion be a key to cfids?

>

> Also, , in terms of excreting metals on one's own, I see from

> Amy's supplement DVD (which I'm now watching) and from the 2006 DVD's,

> that she suggests the (very expensive) charting every week or two with

> urine spot tests. Apparently you fix the methylation cycle, see a peak

> in metals excretion and a return to baseline, and at that point add in

> more 'aggressive' approaches to detox more metals. I assume this is

> what Sue is doing. Anyway, to follow the whole program in an ideal

> mode would be really quite expensive. I guess one (i.e. me) has to

> really pick and choose the supplements. I doubt I can be doing spot

> urines every week. I think they are $55 each? That's what my holistic

> doc remembered.

>

> I do think I'm going to have to spring for one OATS and one urine

> amino acid test. The latter will tell me how to approach taurine.

>

>

>

>

>

>

>

[Guest guest]

Sue, one more question--you did some spot urines before beginning,

right? It isn't the case that for some reason you routinely take in

and dump lots of metals? Dumb question I know but anyway...

I may not start this for a little while. I think I am going to save up

and set aside some $ but also, it turns out, that I decided to

withdraw from my benzo very slowly. I started out going from 30 to 27,

and it was very hard on me. Then I seemed to stabilize and went down

another .3 which I could not 'feel' and yet I think my body is

reacting at the moment. I'm premenstrual but getting chills, sore

glands, and achy, and much more feeling like " I'm going to jump out of

my skin. " I was mystified and upset yesterday then realized that it

may be the benzo reduction.So I'm in for the long haul on the

reduction and maybe will go down about .6 mg per week. WHen I get down

to 20 or 15 I'll probably start beginning Step 1 of her program.

BTW, Rich's point about estrogen is key to me and I want to see if I

have the polymorphisms for trouble processing it. I expect to. I can't

take some things she recommends because of estrogen precursors--such

as curcumin.

> Rich, this question, I could answer for myself if I go

back and read

> all the posts of yours I've printed out, and/or googled some pathways,

> but I thought I'd just ask it anyway.

>

> The ACE deletion--which it turns out I have, Sara probably has, Janet

> has, Sue has...is this in everybody who has taken the Yasko test? If

> so, does this somehow fit in with your high cortisol idea? Because if

> the ACE deletion renders one even more vulnerable to the stress

> response, wouldn't that mean one might have excessively elevated

> cortisol for longer? And couldn't one really crash into fatigue?

>

> Could the ACE deletion be a key to cfids?

>

> Also, , in terms of excreting metals on one's own, I see from

> Amy's supplement DVD (which I'm now watching) and from the 2006 DVD's,

> that she suggests the (very expensive) charting every week or two with

> urine spot tests. Apparently you fix the methylation cycle, see a peak

> in metals excretion and a return to baseline, and at that point add in

> more 'aggressive' approaches to detox more metals. I assume this is

> what Sue is doing. Anyway, to follow the whole program in an ideal

> mode would be really quite expensive. I guess one (i.e. me) has to

> really pick and choose the supplements. I doubt I can be doing spot

> urines every week. I think they are $55 each? That's what my holistic

> doc remembered.

>

> I do think I'm going to have to spring for one OATS and one urine

> amino acid test. The latter will tell me how to approach taurine.

>

>

>

>

>

>

>

[Guest guest]

Thank you very much Rich. I will study this a little myself when I get

a chance and if I find anything interesting will forward to you.

>

> Hi, Jill.

>

> Sorry, I forgot to paste the abstract into my previous post. Here

> it is.

>

> Rich

>

>

> Curr Hypertens Rep. 2000 Apr;2(2):167-73.

>

> Free radical production and angiotensin.

>

> Wolf G.

> University of Hamburg, University Hospital Eppendorf, Department of

> Medicine, Division of Nephrology and Osteology, Pavilion 61,

> istrasse 52, D-20246 Hamburg, Germany. WOLF@...

>

> Angiotensin II (ANG II) has multiple effects on cardiovascular and

> renal cells, including vasoconstriction, cell growth, induction of

> proinflammatory cytokines, and profibrogenic actions. Recent studies

> provide evidence that ANG II could stimulate intracellular formation

> of reactive oxygen species (ROS) such as the superoxide anion (O2-).

> This ANG II-mediated ROS formation exhibits different kinetic and

> lower absolute concentrations than those traditionally observed

> during the respiratory burst of phagocytic cells, but it likely

> involves similar membrane-bound NAD(P)H-oxidases. Current evidence

> suggests that ANG II, through AT1-receptor activation, upregulates

> several subunits of this multienzyme complex, resulting in an

> increase in intracellular O2- concentration. ROS are involved in

> several signal pathways, and redox-sensitive transcriptional factors

> (AP-1, NF-kappaB) have been characterized. ANG II-induced ROS play a

> pivotal role in several pathophysiologic situations of vascular and

> renal cells such as hypertension, endothelial dysfunction, nitrate

> tolerance, atherosclerosis, and cellular remodeling. Although these

> perceptions suggest that drugs interfering with ANG II effects (ACE

> inhibitors, AT1 -receptor antagonist) may serve as antioxidants,

> preventing vascular and renal changes, the clinical studies are not

> so straightforward. In fact, only specific risk groups, such as

> patients with diabetes mellitus or renal insufficiency, may benefit

> from ACE inhibitors, whereas hard endpoints showed no advantage for

> ACE inhibitors in patients with essential hypertension.

>

> PMID: 10981145 [PubMed - indexed for MEDLINE]

>

[Guest guest]

Hi, Jill.

" jill1313 " <jenbooks13@...> wrote:

, in terms of excreting metals on one's own, I see from Amy's supplement

DVD (which I'm now watching) and from the 2006 DVD's, that she suggests the

(very expensive) charting every week or two with urine spot tests. Apparently

you fix the methylation cycle, see a peak in metals excretion and a return to

baseline, and at that point add in

more 'aggressive' approaches to detox more metals.

***Good to know, thanks.

I assume this is what Sue is doing. Anyway, to follow the whole program in an

ideal mode would be really quite expensive. I guess one (i.e. me) has to

really pick and choose the supplements. I doubt I can be doing spot urines every

week. I think they are $55 each?

***That's what I've paid before, yes, but I thought I heard that if one does her

SNP panels or goes through ordering through one of here websites there is a

extra discount on these labs? Yes/No? $55 is the standard cost for Doctor's

Data to do the toxic metals one.

That's what my holistic doc remembered.

I do think I'm going to have to spring for one OATS and one urine

> amino acid test. The latter will tell me how to approach taurine.

>

***Makes sense. I showed great taurine wasting on that one.

[Guest guest]

HI Jill,

I would recommend or on her forum . . they know enough to move

me along 90% of the time . . . the other questions are answered by Dr. Amy.

The forum is wonderful but you do nees to sort through some posts.

Make sure you read all the Sticky notes . . . especially in the " Basics " .

Sue T

jill1313 <jenbooks13@...> wrote:

Thanx Sue that is much appreciated. When I am ready to start Step 1 I

may backchannel you. I did not realize there used to be an extended

GAR available. I do think one could ask questions on site--or research

on site and get some help? Its unfortunate she no longer has time for

that. I wish there were someone extremely smart, the equivalent of a

grad student in a doctoral program, whom she could train.

> Rich, this question, I could answer for myself if I go

back and read

> all the posts of yours I've printed out, and/or googled some pathways,

> but I thought I'd just ask it anyway.

>

> The ACE deletion--which it turns out I have, Sara probably has, Janet

> has, Sue has...is this in everybody who has taken the Yasko test? If

> so, does this somehow fit in with your high cortisol idea? Because if

> the ACE deletion renders one even more vulnerable to the stress

> response, wouldn't that mean one might have excessively elevated

> cortisol for longer? And couldn't one really crash into fatigue?

>

> Could the ACE deletion be a key to cfids?

>

> Also, , in terms of excreting metals on one's own, I see from

> Amy's supplement DVD (which I'm now watching) and from the 2006 DVD's,

> that she suggests the (very expensive) charting every week or two with

> urine spot tests. Apparently you fix the methylation cycle, see a peak

> in metals excretion and a return to baseline, and at that point add in

> more 'aggressive' approaches to detox more metals. I assume this is

> what Sue is doing. Anyway, to follow the whole program in an ideal

> mode would be really quite expensive. I guess one (i.e. me) has to

> really pick and choose the supplements. I doubt I can be doing spot

> urines every week. I think they are $55 each? That's what my holistic

> doc remembered.

>

> I do think I'm going to have to spring for one OATS and one urine

> amino acid test. The latter will tell me how to approach taurine.

>

>

>

>

>

>

>

[Guest guest]

HI JIll,

Nothing was elevated in the beginning of the UTM.

I had a terrible problem coming off Klonopin . . I stilll have Gaba issues

because of it. I think it stirred up lots of mild seizure activity in my brain

and my brain is partially very vulnerable and sensitive because of the

Klonopin.

What is the link between Cucurmin and Estrogen??

Thanks, Sue T

jill1313 <jenbooks13@...> wrote:

Sue, one more question--you did some spot urines before beginning,

right? It isn't the case that for some reason you routinely take in

and dump lots of metals? Dumb question I know but anyway...

I may not start this for a little while. I think I am going to save up

and set aside some $ but also, it turns out, that I decided to

withdraw from my benzo very slowly. I started out going from 30 to 27,

and it was very hard on me. Then I seemed to stabilize and went down

another .3 which I could not 'feel' and yet I think my body is

reacting at the moment. I'm premenstrual but getting chills, sore

glands, and achy, and much more feeling like " I'm going to jump out of

my skin. " I was mystified and upset yesterday then realized that it

may be the benzo reduction.So I'm in for the long haul on the

reduction and maybe will go down about .6 mg per week. WHen I get down

to 20 or 15 I'll probably start beginning Step 1 of her program.

BTW, Rich's point about estrogen is key to me and I want to see if I

have the polymorphisms for trouble processing it. I expect to. I can't

take some things she recommends because of estrogen precursors--such

as curcumin.

> Rich, this question, I could answer for myself if I go

back and read

> all the posts of yours I've printed out, and/or googled some pathways,

> but I thought I'd just ask it anyway.

>

> The ACE deletion--which it turns out I have, Sara probably has, Janet

> has, Sue has...is this in everybody who has taken the Yasko test? If

> so, does this somehow fit in with your high cortisol idea? Because if

> the ACE deletion renders one even more vulnerable to the stress

> response, wouldn't that mean one might have excessively elevated

> cortisol for longer? And couldn't one really crash into fatigue?

>

> Could the ACE deletion be a key to cfids?

>

> Also, , in terms of excreting metals on one's own, I see from

> Amy's supplement DVD (which I'm now watching) and from the 2006 DVD's,

> that she suggests the (very expensive) charting every week or two with

> urine spot tests. Apparently you fix the methylation cycle, see a peak

> in metals excretion and a return to baseline, and at that point add in

> more 'aggressive' approaches to detox more metals. I assume this is

> what Sue is doing. Anyway, to follow the whole program in an ideal

> mode would be really quite expensive. I guess one (i.e. me) has to

> really pick and choose the supplements. I doubt I can be doing spot

> urines every week. I think they are $55 each? That's what my holistic

> doc remembered.

>

> I do think I'm going to have to spring for one OATS and one urine

> amino acid test. The latter will tell me how to approach taurine.

>

>

>

>

>

>

>

[Guest guest]

Sue,

How much klonopin were you taking? I was wondering why you think it stirred up

seizure activity? And gave you Gaba issues...what does that mean, and feel like?

Is there something that can help, as in taking GABA?

I took Neurontin for several years. For the 1st couple I think it really

improved cognitive function and nerve pain. Later, it's hard to explain, but I

came to hate being on it and went off slowly. It felt like it took forever to

leave my system if it even did.

If ever in extended stress period, tho, I might take small amounts temporarily,

because I know it would help.

What are you taking as the 1st part of Step 2 and to support the Mitochondria?

Do you still take everything from Step 1?

Thanks,

Katrina

> > Rich, this question, I could answer for myself if I go

> back and read

> > all the posts of yours I've printed out, and/or googled some pathways,

> > but I thought I'd just ask it anyway.

> >

> > The ACE deletion--which it turns out I have, Sara probably has, Janet

> > has, Sue has...is this in everybody who has taken the Yasko test? If

> > so, does this somehow fit in with your high cortisol idea? Because if

> > the ACE deletion renders one even more vulnerable to the stress

> > response, wouldn't that mean one might have excessively elevated

> > cortisol for longer? And couldn't one really crash into fatigue?

> >

> > Could the ACE deletion be a key to cfids?

> >

> > Also, , in terms of excreting metals on one's own, I see from

> > Amy's supplement DVD (which I'm now watching) and from the 2006 DVD's,

> > that she suggests the (very expensive) charting every week or two with

> > urine spot tests. Apparently you fix the methylation cycle, see a peak

> > in metals excretion and a return to baseline, and at that point add in

> > more 'aggressive' approaches to detox more metals. I assume this is

> > what Sue is doing. Anyway, to follow the whole program in an ideal

> > mode would be really quite expensive. I guess one (i.e. me) has to

> > really pick and choose the supplements. I doubt I can be doing spot

> > urines every week. I think they are $55 each? That's what my holistic

> > doc remembered.

> >

> > I do think I'm going to have to spring for one OATS and one urine

> > amino acid test. The latter will tell me how to approach taurine.

> >

> >

> >

> >

> >

> >

> >

[Guest guest]

kattemayo <kattemayo@...> wrote:Sue,

How much klonopin were you taking?

***** 1 mg then .5 for awhile.

I was wondering why you think it stirred up seizure activity? And gave you

Gaba issues...what does that mean, and feel like? Is there something that can

help, as in taking GABA?

****Static in brain, eye flshing at night, poor sleep, etc. Gavba helps alot

.. . . it is my substitue to Klonopin

I took Neurontin for several years. For the 1st couple I think it really

improved cognitive function and nerve pain. Later, it's hard to explain, but I

came to hate being on it and went off slowly. It felt like it took forever to

leave my system if it even did.

If ever in extended stress period, tho, I might take small amounts temporarily,

because I know it would help.

What are you taking as the 1st part of Step 2 and to support the Mitochondria?

Do you still take everything from Step 1?

****Yes . . . I do take everything in step one . . and 70% of Step 2 listed

in her book " The Puzzle of Autism . .Putting it all together " . I can't list the

60+ supplements . . they may be very differenent for you. PLease get and read

the book . . . very important for supplement info. Sorry it is too much to post.

Thanks,

Katrina

[Guest guest]

Sue, how long were you on klonipin, what dose, and did you taper off

by cuts or water titration? I'm noticing some strange unexpected stuff

on slowly tapering off temazapem. The first " cut " of 3 milligrams was

awful for about five to six days, purely awful. Then my body seemed to

stabilize and so I cut only .3 (2 ml) out of the night time dose. And

I didn't notice anything at all, and slept normally, EXCEPT my

behavior is not exactly normal. I release in some way I am

disinhibited, I just realized it today, that aggression and anxiety

are higher than normal (although, before any benzo, I tended to excess

esp. on anxiety, which is inherited as far as I can see. So for me,

maybe a little bit of benzo, a small amount, i.e. a few milligrams, is

not such a bad idea. Who knows).

I didn't recognize this as withdrawal until today. ALSO, I'm getting

sick along with PMS. I have read that withdrawing from benzos can make

you more vulnerable to flus.

Curcumin--like many other herbs and plants--has estrogenic-like

compounds. I have to be very careful. Either I have excess estrogens

from a systemic fungal infection and/or I don't detox them well, per

Rich's point about that one polymorphism.

-- In , Sue T <morabshadow@...> wrote:

>

> HI JIll,

>

> Nothing was elevated in the beginning of the UTM.

> I had a terrible problem coming off Klonopin . . I stilll have

Gaba issues because of it. I think it stirred up lots of mild seizure

activity in my brain and my brain is partially very vulnerable and

sensitive because of the Klonopin.

>

> What is the link between Cucurmin and Estrogen??

>

> Thanks, Sue T

>

>

> jill1313 <jenbooks13@...> wrote:

> Sue, one more question--you did some spot urines before

beginning,

> right? It isn't the case that for some reason you routinely take in

> and dump lots of metals? Dumb question I know but anyway...

>

> I may not start this for a little while. I think I am going to save up

> and set aside some $ but also, it turns out, that I decided to

> withdraw from my benzo very slowly. I started out going from 30 to 27,

> and it was very hard on me. Then I seemed to stabilize and went down

> another .3 which I could not 'feel' and yet I think my body is

> reacting at the moment. I'm premenstrual but getting chills, sore

> glands, and achy, and much more feeling like " I'm going to jump out of

> my skin. " I was mystified and upset yesterday then realized that it

> may be the benzo reduction.So I'm in for the long haul on the

> reduction and maybe will go down about .6 mg per week. WHen I get down

> to 20 or 15 I'll probably start beginning Step 1 of her program.

>

> BTW, Rich's point about estrogen is key to me and I want to see if I

> have the polymorphisms for trouble processing it. I expect to. I can't

> take some things she recommends because of estrogen precursors--such

> as curcumin.

>

>

> > Rich, this question, I could answer for myself if I go

> back and read

> > all the posts of yours I've printed out, and/or googled some pathways,

> > but I thought I'd just ask it anyway.

> >

> > The ACE deletion--which it turns out I have, Sara probably has, Janet

> > has, Sue has...is this in everybody who has taken the Yasko test? If

> > so, does this somehow fit in with your high cortisol idea? Because if

> > the ACE deletion renders one even more vulnerable to the stress

> > response, wouldn't that mean one might have excessively elevated

> > cortisol for longer? And couldn't one really crash into fatigue?

> >

> > Could the ACE deletion be a key to cfids?

> >

> > Also, , in terms of excreting metals on one's own, I see from

> > Amy's supplement DVD (which I'm now watching) and from the 2006 DVD's,

> > that she suggests the (very expensive) charting every week or two with

> > urine spot tests. Apparently you fix the methylation cycle, see a peak

> > in metals excretion and a return to baseline, and at that point add in

> > more 'aggressive' approaches to detox more metals. I assume this is

> > what Sue is doing. Anyway, to follow the whole program in an ideal

> > mode would be really quite expensive. I guess one (i.e. me) has to

> > really pick and choose the supplements. I doubt I can be doing spot

> > urines every week. I think they are $55 each? That's what my holistic

> > doc remembered.

> >

> > I do think I'm going to have to spring for one OATS and one urine

> > amino acid test. The latter will tell me how to approach taurine.

> >

> >

> >

> >

> >

> >

> >

[Guest guest]

Hi Jill,

> >

> >

[Guest guest]

>there is evidence that angiotensin II increases the production of

oxidizing free radicals

So there might really be a benefit to Angiotensin receptor blockers like

Benicar?

++PLS

rvankonynen wrote:

> Hi, Jill.

>

> Out of nine PWCs for whom I now have these data, eight are

> homozygous for ACE (deletion 16), and one is homozygous for ACE

> (inclusion 16).

>

> The ACE deletion SNP would tend to raise the secretion of

> aldosterone by the adrenals, but I don't think it would affect

> cortisol secretion. However, it raises the level of angiotensisn

> II, and there is evidence that angiotensin II increases the

> production of oxidizing free radicals. See abstract below. So

> maybe its role in biasing a person toward developing CFS is that it

> stacks one more straw on the camel's back in the direction of

> producing oxidative stress, and thus depleting glutathione, just as

> I suspect the CYP1B1 SNP does in women, in detoxing estradiol.

>

> More and more, based on what I'm seeing, my motto is

> becoming, " Follow the glutathione. "

>

> Rich

>

[Guest guest]

Hi, .

For people who have the ACE upregulation SNP, perhaps so. ACE

inhibitors might be considered as well. Oxidative stress is one of

the best documented biochemical features of CFS. Anything that

would tend to pull a person back from that might have potential

benefit. Here's an abstract that might be interesting:

Curr Hypertens Rep. 2000 Apr;2(2):167-73.

Free radical production and angiotensin.

Wolf G.

University of Hamburg, University Hospital Eppendorf, Department of

Medicine, Division of Nephrology and Osteology, Pavilion 61,

istrasse 52, D-20246 Hamburg, Germany. WOLF@...

Angiotensin II (ANG II) has multiple effects on cardiovascular and

renal cells, including vasoconstriction, cell growth, induction of

proinflammatory cytokines, and profibrogenic actions. Recent studies

provide evidence that ANG II could stimulate intracellular formation

of reactive oxygen species (ROS) such as the superoxide anion (O2-).

This ANG II-mediated ROS formation exhibits different kinetic and

lower absolute concentrations than those traditionally observed

during the respiratory burst of phagocytic cells, but it likely

involves similar membrane-bound NAD(P)H-oxidases. Current evidence

suggests that ANG II, through AT1-receptor activation, upregulates

several subunits of this multienzyme complex, resulting in an

increase in intracellular O2- concentration. ROS are involved in

several signal pathways, and redox-sensitive transcriptional factors

(AP-1, NF-kappaB) have been characterized. ANG II-induced ROS play a

pivotal role in several pathophysiologic situations of vascular and

renal cells such as hypertension, endothelial dysfunction, nitrate

tolerance, atherosclerosis, and cellular remodeling. Although these

perceptions suggest that drugs interfering with ANG II effects (ACE

inhibitors, AT1 -receptor antagonist) may serve as antioxidants,

preventing vascular and renal changes, the clinical studies are not

so straightforward. In fact, only specific risk groups, such as

patients with diabetes mellitus or renal insufficiency, may benefit

from ACE inhibitors, whereas hard endpoints showed no advantage for

ACE inhibitors in patients with essential hypertension.

PMID: 10981145 [PubMed - indexed for MEDLINE]

Rich

> > Hi, Jill.

> >

> > Out of nine PWCs for whom I now have these data, eight are

> > homozygous for ACE (deletion 16), and one is homozygous for ACE

> > (inclusion 16).

> >

> > The ACE deletion SNP would tend to raise the secretion of

> > aldosterone by the adrenals, but I don't think it would affect

> > cortisol secretion. However, it raises the level of

angiotensisn

> > II, and there is evidence that angiotensin II increases the

> > production of oxidizing free radicals. See abstract below. So

> > maybe its role in biasing a person toward developing CFS is that

it

> > stacks one more straw on the camel's back in the direction of

> > producing oxidative stress, and thus depleting glutathione, just

as

> > I suspect the CYP1B1 SNP does in women, in detoxing estradiol.

> >

> > More and more, based on what I'm seeing, my motto is

> > becoming, " Follow the glutathione. "

> >

> > Rich

> >

>

[Guest guest]

Rich, I want to sit in with you in early Oct when you ask Amy all your

questions.

I read that paper. Okay, that is the first thing I've read that gives

some credence to the infamous unnamed protocol that I myself totally

avoided.

THis may sound silly, but avoiding stress is very important if you

have an ACE mutation. That should probably be the first thing we

do--meditate, learn not to have a large stress response.

Then, I am naturally inclined AWAY from drugs so there may be gentle

ways to modulate this pathway through herbs enzymes etc. Interesting

that they noted that infection renders tissue hypoxic------another

point in favor of hyperbaric oxygen, or living at sea level. That

article was quite surprising in how it related ACE to so many modern

diseases.

> > > Hi, Jill.

> > >

> > > Out of nine PWCs for whom I now have these data, eight are

> > > homozygous for ACE (deletion 16), and one is homozygous for ACE

> > > (inclusion 16).

> > >

> > > The ACE deletion SNP would tend to raise the secretion of

> > > aldosterone by the adrenals, but I don't think it would affect

> > > cortisol secretion. However, it raises the level of

> angiotensisn

> > > II, and there is evidence that angiotensin II increases the

> > > production of oxidizing free radicals. See abstract below. So

> > > maybe its role in biasing a person toward developing CFS is that

> it

> > > stacks one more straw on the camel's back in the direction of

> > > producing oxidative stress, and thus depleting glutathione, just

> as

> > > I suspect the CYP1B1 SNP does in women, in detoxing estradiol.

> > >

> > > More and more, based on what I'm seeing, my motto is

> > > becoming, " Follow the glutathione. "

> > >

> > > Rich

> > >

> >

>

[Guest guest]

Whoa, hold on there and Rich!

Benicar is a bad idea for PWCs and perhaps many other illnesses where oxidative

stress plays a key role.

Check this out.

Benicar blocks angiotensin II(ang II)receptors, right? But it doesn't cross the

blood-brain barrier(BBB) to provide this same service!

Bingo! This is a big rub with Benicar for PWCs!

PWCs have oxidative stress and noted extrapermiable BBBs, but with Benicar use

where would all the blocked ang II in the body have a chance to go to attach to

unblocked ang II receptors to do its bidding, vasoconstruction as it's known to

do and possibly increase oxidative stress?

That already BBB permiable, oxidatively stressed and microvascularly tortured(ie

Hyde) PWC brain is the answer! Be clear, I'm not saying Benicar passes the BBB,

even if permiable, but it is all that ang II floating around as a result of

being blocked by Benicar in the body that can cross into and I believe has

crossed into PWC brains to attach to their unblocked ang II receptors there.

This potential was noted by Cheney publicly in 2004-2005 and it is has been my

personal experience as well. Within a matter of days after starting the, banned

in name on this list, experimental treatment for CFS with Benicar as its primary

tool, I came down with right side cervical(neck) dystonia, which I had never had

before and which has not abaded now almost two years later.

Dystonia most obviously affects muscles, but it is in origin a basal ganglia

brain disorder, and as you may have read in my case as well as other PWCs,

abnormal function with the basal ganglia as well as the right hippocampus, which

there is brain MRS evidence showing abnormal metabolism, have been specifically

suggested by CFS researchers. These dysfunctions in CFS are quite arguably

oxidative stress induced.

Benicar is a danger to making these problems and cases of CFS worse.

Schauble <pls2@...> wrote:

>

> >there is evidence that angiotensin II increases the production of

> oxidizing free radicals

>

> So there might really be a benefit to Angiotensin receptor blockers like

> Benicar?

>

> ++PLS

>

[Guest guest]

Hi, Jill.

It's going to be the latter part of October, and I think the way it

will work is that I will email her questions from this group (and

myself), and she will send her responses, which I will post. So in

that sense, we will all be " sitting in. "

Thanks for your comments on that paper. I was surprised, too, and I

share your proclivity toward nonpharmaceutical solutions, if

possible.

Rich

> > > > Hi, Jill.

> > > >

> > > > Out of nine PWCs for whom I now have these data, eight are

> > > > homozygous for ACE (deletion 16), and one is homozygous for

ACE

> > > > (inclusion 16).

> > > >

> > > > The ACE deletion SNP would tend to raise the secretion of

> > > > aldosterone by the adrenals, but I don't think it would

affect

> > > > cortisol secretion. However, it raises the level of

> > angiotensisn

> > > > II, and there is evidence that angiotensin II increases the

> > > > production of oxidizing free radicals. See abstract below.

So

> > > > maybe its role in biasing a person toward developing CFS is

that

> > it

> > > > stacks one more straw on the camel's back in the direction

of

> > > > producing oxidative stress, and thus depleting glutathione,

just

> > as

> > > > I suspect the CYP1B1 SNP does in women, in detoxing

estradiol.

> > > >

> > > > More and more, based on what I'm seeing, my motto is

> > > > becoming, " Follow the glutathione. "

> > > >

> > > > Rich

> > > >

> > >

> >

>

[Guest guest]

Sorry Rich. I was thinking of the conference.

> > > > > Hi, Jill.

> > > > >

> > > > > Out of nine PWCs for whom I now have these data, eight are

> > > > > homozygous for ACE (deletion 16), and one is homozygous for

> ACE

> > > > > (inclusion 16).

> > > > >

> > > > > The ACE deletion SNP would tend to raise the secretion of

> > > > > aldosterone by the adrenals, but I don't think it would

> affect

> > > > > cortisol secretion. However, it raises the level of

> > > angiotensisn

> > > > > II, and there is evidence that angiotensin II increases the

> > > > > production of oxidizing free radicals. See abstract below.

> So

> > > > > maybe its role in biasing a person toward developing CFS is

> that

> > > it

> > > > > stacks one more straw on the camel's back in the direction

> of

> > > > > producing oxidative stress, and thus depleting glutathione,

> just

> > > as

> > > > > I suspect the CYP1B1 SNP does in women, in detoxing

> estradiol.

> > > > >

> > > > > More and more, based on what I'm seeing, my motto is

> > > > > becoming, " Follow the glutathione. "

> > > > >

> > > > > Rich

> > > > >

> > > >

> > >

> >

>

[Guest guest]

Hi, .

Thank you for sharing your experience and insights. As you know, I

am not a big fan of pharmaceuticals in general, and I'm not going to

defend the use of this one. I'm sorry it caused you problems that

have hung on. As I said in a message to Jill earlier, I agree that

nonpharmaceutical approaches are to be preferred when possible.

Rich

>

> Whoa, hold on there and Rich!

>

>

>

> Benicar is a bad idea for PWCs and perhaps many other illnesses

where oxidative stress plays a key role.

> Check this out.

>

>

>

> Benicar blocks angiotensin II(ang II)receptors, right? But it

doesn't cross the blood-brain barrier(BBB) to provide this same

service!

>

>

>

> Bingo! This is a big rub with Benicar for PWCs!

>

>

>

> PWCs have oxidative stress and noted extrapermiable BBBs, but with

Benicar use where would all the blocked ang II in the body have a

chance to go to attach to unblocked ang II receptors to do its

bidding, vasoconstruction as it's known to do and possibly increase

oxidative stress?

>

>

>

> That already BBB permiable, oxidatively stressed and

microvascularly tortured(ie Hyde) PWC brain is the answer! Be

clear, I'm not saying Benicar passes the BBB, even if permiable, but

it is all that ang II floating around as a result of being blocked

by Benicar in the body that can cross into and I believe has crossed

into PWC brains to attach to their unblocked ang II receptors there.

>

>

>

> This potential was noted by Cheney publicly in 2004-2005 and it is

has been my personal experience as well. Within a matter of days

after starting the, banned in name on this list, experimental

treatment for CFS with Benicar as its primary tool, I came down with

right side cervical(neck) dystonia, which I had never had before and

which has not abaded now almost two years later.

>

>

>

> Dystonia most obviously affects muscles, but it is in origin a

basal ganglia brain disorder, and as you may have read in my case as

well as other PWCs, abnormal function with the basal ganglia as well

as the right hippocampus, which there is brain MRS evidence showing

abnormal metabolism, have been specifically suggested by CFS

researchers. These dysfunctions in CFS are quite arguably oxidative

stress induced.

>

>

>

> Benicar is a danger to making these problems and cases of CFS

worse.

>

>

>

>

[Guest guest]

Hi, Rich.

A bit more on the ang II issue is I just spotted in my lab tests

and recalled that I have a

GNB3(825C-T) +/+ SNP. This SNP according to Genovations, besides being linked

to increased risked for depression and bipolar disorder(which I don't have so

far, IMO), facilitates the action of ang II in vasoconstriction.

So, perhaps this makes me that much more vulnerable to having a bad side effect

like the dystonia I got from Benicar. In 2002, Dr Cheney thought the fact that I

had the typical low blood pressure common to PWCs that this counterbalanced what

my GNB3 SNP could do, but now it also seems to my understanding, and perhaps

more importantly, that it could be another SNP to look out for that could with

ACE deletions and the other SNPs being found in CFS/autism result in low

glutathione/oxidative stress.

" rvankonynen " <richvank@...> wrote:

>

> Hi, .

>

> Thank you for sharing your experience and insights. As you know, I

> am not a big fan of pharmaceuticals in general, and I'm not going to

> defend the use of this one. I'm sorry it caused you problems that

> have hung on. As I said in a message to Jill earlier, I agree that

> nonpharmaceutical approaches are to be preferred when possible.

>

> Rich

> <davidhall@> wrote:

I'm not saying Benicar passes the BBB, even if permiable, but

> it is all that ang II floating around as a result of being blocked

> by Benicar in the body that can cross into and I believe has crossed

> into PWC brains to attach to their unblocked ang II receptors there....This

potential was noted by Cheney publicly in 2004-2005 and it is

> has been my personal experience as well....Benicar is a danger to making these

problems and cases of CFS

> worse.

> >

> >

> >

> >