RE: Major discussion, thoughts on trypophan, BCAA, LDN etc..

July 29, 2005

, I'd love to hear how men can get PCOS when they have no ovaries?

Rosie

Subject: Major discussion, thoughts on trypophan,

BCAA, LDN etc..

Dear everyone,

I research 24/7 on every single resource on the net, people etc.. so

I have gathered far too much information for my brain to handle. I

would love to write up articles/research for magazines/newsletters

or what not but I guess I feel like I just come off too complicated.

If anyone has any ideas, suggestions or would like to work with me

on research or anything, i would be delighted.

(fibromyalgia@...)

Just some random thoughts and conversations :

There is a common pattern I do see more and more. I won't put

anything together in concrete since CFS is like mud anyways, but

these seem to overlap with CFS often and relate to strange

similiarities :

1) polycystic ovary syndrome (in men and women - and yes men can get

it too) I really do think many of us men and women have a form of

PCOS undignosed. Metformin (Glucophage), diet excersize, may help.

Ill note that low dose naltrexone has wowwly changed my

glucose/insulin or something. I notice major changed now, for the

better - i seem to assimilate foods better etc...

2) Ok, in men only - androgentic alopecia (baldness). Caused by

excess sensitvity of androgen receptors in the scalp, therefore DHT

(dihydrotestosterone) basically destroys it. believe it or not, I've

researched hair loss for years for my own hair (LOL) and it has VERY

similar patterns in hormones to CFS/ PCOS. I highly suspect the

hormone axis (DHEA/testosterone/DHT/all estrogens) is very messed up

in CFS and there may be a common pattern to one of our main

subgroups. In addition I am 75% sure that MPB is truly caused by an

increased sensitvity to stress or perhaps an evolutionary resistance

to it. Stress is somehow related like this -> 5 alpha reductase

degrades testosterone into DHT, but also it functions(degrades) to

create a long protein which i dont feel like spelling, but basically

its " allpregnanolone " . This protein functions to modulate GABA-A

receptor senstivity as far as science knows. GABA-A = stress power.

So truly, stress can probably cause alopecia in men. And I have also

theorized that since women don't possess this " stress resistance "

function (ie they dont really bald etc etc) this is why they are

more susceptable to autoimmune disease : decreased ability

to " modulate stress " . This is all in my head, no offense attended

women. I would love someone to try to fix, help, or invalidate my

theory.

2) insulin resistance (which in my example here related to carb.

intake and the depletion of isolecuine/leucine *BCAA*. An example,

of course.

3) tryptophan catabolism once again - we get quinolinic acid (but

we sorta need it) and then the good guy to protect our NMDA's ->

kynurenic acid. This whole pathway is highly implicated in

huntingtons disease (and others) and we do have the proteins

expressing the huntingin factor... its messed up in CFS IMO.

4) Biggest issue -> melatonin -> synthesized from serotonin which

takes 2 steps utilizing the acetyl from -> " acetyl-CoA " and a methyl

group from " SAME " (S-AdenosylMethionine) CFS patients have major

melatonin problems and defiencys of SAME and many other aminos,

peptides & the building blocks for some of these steps , which IMO

points to alterted tryptophan metabolism for some reason, upstream

probably. Remember tryptophan is primiarly in the GUT so diet will

effect it. Sleep problems I really do think relate to this somehow.

5)Branched Chained Amino Acids are Depleted in CFS. Just tonight I

made a startling discovery : BCAA's somehow either " bind " " use " or

are related to enkephalin and endorphins . The prime example :

Leucine enkephalin. So we got BCAA's being used up, endorphins

(probably being used up - based on the 3 pubmed studies showing low

bendorphin levels and general speculation honestly)

6)BCAA's could maybe be binding with endorphins for some purpose?

Protecting us? who knows? " Leucine-enkephalin "

7) Low dose naltrexone at 3.0-4.5 ONLY blocks the MU-opiod receptors

for about 4 hours at nighttime when the glands produce the

endorphins, enkephalins for the day. The temp. block tricks the body

into making more of both. This means BCAA's or anything that needs

endorphins has far more availbility, unlike before in which studies

consistently prove low endorphin levels in nearly all chronic

diseases, especially autoimmune, and this includes CFS and FM. Check

medline. I imagine we are just hitting somewhere down the line with

LDN. The body is SOOOO complex, endorphins may be in the middle, or

on the top, but they are in our path and they do work for many

diseases, especially MS, which I will 99% say will stop MS

progression just to show my confidence in LDN.

So the question is : where is LDN , in this complex process,

altering the variables. My DHEA/testerone/DHT is clearly up as I

have taken DHEA before and went through pubuerty, the effects are

nearly identical. I am in stage 1 of cheneys chart though, so there

are so many variables vs other CFS people. I am also young, 22.

Comments, Thoughts, Criticizms?

Sorry for spelling, its late, tired!

Constructive crticism if you must also.

P.S. I am still looking for a job (volunteer etc).

JL

fibromyalgia@...

This list is intended for patients to share personal experiences with

each other, not to give medical advice. If you are interested in any

treatment discussed here, please consult your doctor.

July 29, 2005

That opportunity awaits you at CFS Phoenix. That website was created with the

hope that patients who wanted to do overviews of specific research topics could

contribute to it. So far Rich has contributed several papers and a

contributed her overview of the lasted AACFS conference but thats it. Dont worry

about being too complicated - these are very complex topics and some real

complexity is unavoidable. Just try to make it as clear and organized as

possible.

A paper put up on the website will stay there - giving it a life that will

extend far beyond any discussions on the chat group.

http://phoenix-cfs.org/The%20SITE/SubmitPaper.htm

jasonlbreckenridge wrote:

> Dear everyone,

>

> I research 24/7 on every single resource on the net, people etc.. so

> I have gathered far too much information for my brain to handle. I

> would love to write up articles/research for magazines/newsletters

> or what not but I guess I feel like I just come off too complicated.

> If anyone has any ideas, suggestions or would like to work with me

> on research or anything, i would be delighted.

> (fibromyalgia@...)

>

> Just some random thoughts and conversations :

>

> There is a common pattern I do see more and more. I won't put

> anything together in concrete since CFS is like mud anyways, but

> these seem to overlap with CFS often and relate to strange

> similiarities :

>

> 1) polycystic ovary syndrome (in men and women - and yes men can get

> it too) I really do think many of us men and women have a form of

> PCOS undignosed. Metformin (Glucophage), diet excersize, may help.

> Ill note that low dose naltrexone has wowwly changed my

> glucose/insulin or something. I notice major changed now, for the

> better - i seem to assimilate foods better etc...

>

> 2) Ok, in men only - androgentic alopecia (baldness). Caused by

> excess sensitvity of androgen receptors in the scalp, therefore DHT

> (dihydrotestosterone) basically destroys it. believe it or not, I've

> researched hair loss for years for my own hair (LOL) and it has VERY

> similar patterns in hormones to CFS/ PCOS. I highly suspect the

> hormone axis (DHEA/testosterone/DHT/all estrogens) is very messed up

> in CFS and there may be a common pattern to one of our main

> subgroups. In addition I am 75% sure that MPB is truly caused by an

> increased sensitvity to stress or perhaps an evolutionary resistance

> to it. Stress is somehow related like this -> 5 alpha reductase

> degrades testosterone into DHT, but also it functions(degrades) to

> create a long protein which i dont feel like spelling, but basically

> its " allpregnanolone " . This protein functions to modulate GABA-A

> receptor senstivity as far as science knows. GABA-A = stress power.

> So truly, stress can probably cause alopecia in men. And I have also

> theorized that since women don't possess this " stress resistance "

> function (ie they dont really bald etc etc) this is why they are

> more susceptable to autoimmune disease : decreased ability

> to " modulate stress " . This is all in my head, no offense attended

> women. I would love someone to try to fix, help, or invalidate my

> theory.

>

> 2) insulin resistance (which in my example here related to carb.

> intake and the depletion of isolecuine/leucine *BCAA*. An example,

> of course.

>

> 3) tryptophan catabolism once again - we get quinolinic acid (but

> we sorta need it) and then the good guy to protect our NMDA's ->

> kynurenic acid. This whole pathway is highly implicated in

> huntingtons disease (and others) and we do have the proteins

> expressing the huntingin factor... its messed up in CFS IMO.

>

> 4) Biggest issue -> melatonin -> synthesized from serotonin which

> takes 2 steps utilizing the acetyl from -> " acetyl-CoA " and a methyl

> group from " SAME " (S-AdenosylMethionine) CFS patients have major

> melatonin problems and defiencys of SAME and many other aminos,

> peptides & the building blocks for some of these steps , which IMO

> points to alterted tryptophan metabolism for some reason, upstream

> probably. Remember tryptophan is primiarly in the GUT so diet will

> effect it. Sleep problems I really do think relate to this somehow.

>

> 5)Branched Chained Amino Acids are Depleted in CFS. Just tonight I

> made a startling discovery : BCAA's somehow either " bind " " use " or

> are related to enkephalin and endorphins . The prime example :

> Leucine enkephalin. So we got BCAA's being used up, endorphins

> (probably being used up - based on the 3 pubmed studies showing low

> bendorphin levels and general speculation honestly)

>

> 6)BCAA's could maybe be binding with endorphins for some purpose?

> Protecting us? who knows? " Leucine-enkephalin "

>

> 7) Low dose naltrexone at 3.0-4.5 ONLY blocks the MU-opiod receptors

> for about 4 hours at nighttime when the glands produce the

> endorphins, enkephalins for the day. The temp. block tricks the body

> into making more of both. This means BCAA's or anything that needs

> endorphins has far more availbility, unlike before in which studies

> consistently prove low endorphin levels in nearly all chronic

> diseases, especially autoimmune, and this includes CFS and FM. Check

> medline. I imagine we are just hitting somewhere down the line with

> LDN. The body is SOOOO complex, endorphins may be in the middle, or

> on the top, but they are in our path and they do work for many

> diseases, especially MS, which I will 99% say will stop MS

> progression just to show my confidence in LDN.

>

> So the question is : where is LDN , in this complex process,

> altering the variables. My DHEA/testerone/DHT is clearly up as I

> have taken DHEA before and went through pubuerty, the effects are

> nearly identical. I am in stage 1 of cheneys chart though, so there

> are so many variables vs other CFS people. I am also young, 22.

>

> Comments, Thoughts, Criticizms?

>

> Sorry for spelling, its late, tired!

>

> Constructive crticism if you must also.

>

> P.S. I am still looking for a job (volunteer etc).

>

> JL

> fibromyalgia@...

July 29, 2005

Polycystic ovary syndrome is somewhat of an incorrect name actually.

THE PCOS is an effect, not the cause. The cause is excess andogens

with related insulin resistance problems, very common in CFS. So yes

men can have PCOS, it is documented on medline. They should probably

change the name though..

> , I'd love to hear how men can get PCOS when they have no

ovaries?

>

> Rosie

>

> Subject: Major discussion, thoughts on

trypophan,

> BCAA, LDN etc..

>

> Dear everyone,

>

> I research 24/7 on every single resource on the net, people etc..

so

> I have gathered far too much information for my brain to handle. I

> would love to write up articles/research for magazines/newsletters

> or what not but I guess I feel like I just come off too

complicated.

> If anyone has any ideas, suggestions or would like to work with me

> on research or anything, i would be delighted.

> (fibromyalgia@g...)

>

> Just some random thoughts and conversations :

>

> There is a common pattern I do see more and more. I won't put

> anything together in concrete since CFS is like mud anyways, but

> these seem to overlap with CFS often and relate to strange

> similiarities :

>

> 1) polycystic ovary syndrome (in men and women - and yes men can

get

> it too) I really do think many of us men and women have a form of

> PCOS undignosed. Metformin (Glucophage), diet excersize, may help.

> Ill note that low dose naltrexone has wowwly changed my

> glucose/insulin or something. I notice major changed now, for the

> better - i seem to assimilate foods better etc...

>

> 2) Ok, in men only - androgentic alopecia (baldness). Caused by

> excess sensitvity of androgen receptors in the scalp, therefore

DHT

> (dihydrotestosterone) basically destroys it. believe it or not,

I've

> researched hair loss for years for my own hair (LOL) and it has

VERY

> similar patterns in hormones to CFS/ PCOS. I highly suspect the

> hormone axis (DHEA/testosterone/DHT/all estrogens) is very messed

up

> in CFS and there may be a common pattern to one of our main

> subgroups. In addition I am 75% sure that MPB is truly caused by

an

> increased sensitvity to stress or perhaps an evolutionary

resistance

> to it. Stress is somehow related like this -> 5 alpha reductase

> degrades testosterone into DHT, but also it functions(degrades) to

> create a long protein which i dont feel like spelling, but

basically

> its " allpregnanolone " . This protein functions to modulate GABA-A

> receptor senstivity as far as science knows. GABA-A = stress

power.

> So truly, stress can probably cause alopecia in men. And I have

also

> theorized that since women don't possess this " stress resistance "

> function (ie they dont really bald etc etc) this is why they are

> more susceptable to autoimmune disease : decreased ability

> to " modulate stress " . This is all in my head, no offense attended

> women. I would love someone to try to fix, help, or invalidate my

> theory.

>

> 2) insulin resistance (which in my example here related to carb.

> intake and the depletion of isolecuine/leucine *BCAA*. An example,

> of course.

>

> 3) tryptophan catabolism once again - we get quinolinic acid (but

> we sorta need it) and then the good guy to protect our NMDA's ->

> kynurenic acid. This whole pathway is highly implicated in

> huntingtons disease (and others) and we do have the proteins

> expressing the huntingin factor... its messed up in CFS IMO.

>

> 4) Biggest issue -> melatonin -> synthesized from serotonin which

> takes 2 steps utilizing the acetyl from -> " acetyl-CoA " and a

methyl

> group from " SAME " (S-AdenosylMethionine) CFS patients have major

> melatonin problems and defiencys of SAME and many other aminos,

> peptides & the building blocks for some of these steps , which IMO

> points to alterted tryptophan metabolism for some reason, upstream

> probably. Remember tryptophan is primiarly in the GUT so diet will

> effect it. Sleep problems I really do think relate to this somehow.

>

> 5)Branched Chained Amino Acids are Depleted in CFS. Just tonight I

> made a startling discovery : BCAA's somehow either " bind " " use " or

> are related to enkephalin and endorphins . The prime example :

> Leucine enkephalin. So we got BCAA's being used up, endorphins

> (probably being used up - based on the 3 pubmed studies showing

low

> bendorphin levels and general speculation honestly)

>

> 6)BCAA's could maybe be binding with endorphins for some purpose?

> Protecting us? who knows? " Leucine-enkephalin "

>

> 7) Low dose naltrexone at 3.0-4.5 ONLY blocks the MU-opiod

receptors

> for about 4 hours at nighttime when the glands produce the

> endorphins, enkephalins for the day. The temp. block tricks the

body

> into making more of both. This means BCAA's or anything that needs

> endorphins has far more availbility, unlike before in which

studies

> consistently prove low endorphin levels in nearly all chronic

> diseases, especially autoimmune, and this includes CFS and FM.

Check

> medline. I imagine we are just hitting somewhere down the line

with

> LDN. The body is SOOOO complex, endorphins may be in the middle,

or

> on the top, but they are in our path and they do work for many

> diseases, especially MS, which I will 99% say will stop MS

> progression just to show my confidence in LDN.

>

> So the question is : where is LDN , in this complex process,

> altering the variables. My DHEA/testerone/DHT is clearly up as I

> have taken DHEA before and went through pubuerty, the effects are

> nearly identical. I am in stage 1 of cheneys chart though, so

there

> are so many variables vs other CFS people. I am also young, 22.

>

> Comments, Thoughts, Criticizms?

>

> Sorry for spelling, its late, tired!

>

> Constructive crticism if you must also.

>

> P.S. I am still looking for a job (volunteer etc).

>

> JL

> fibromyalgia@g...

>

> This list is intended for patients to share personal experiences

with

> each other, not to give medical advice. If you are interested in

any

> treatment discussed here, please consult your doctor.

>

July 29, 2005

,

<>How can men have PCOS if the don't have ovaries?

Hair loss can be caused by iron deficiency, adrenal function problem,

PCOS, hypothyroidism, fungal infection of scalp, vitamin C deficiency,

biotin deficiency, S.L.E., EFA deficiency, excess vitamin A, high

copper, zinc deficiency, excess androgens in females, excess estrogen in

men, estrogen dominance in females, testosterone deficiency in females,

low B12, parasites, cadmium, excess selenium, vitamin D receptor

polymorphism, thallium. Many of these things are common in CFS.

Don't forget that adipose tissue converts testosterone to DHT.

The relationship between insulin and dietary protein is complex. On one

hand some amino acids increase insulin sensitivity, on the other hand

dietary protein increases insulin secretion.

I actually did a literature review earlier this year of every paper I

could find measuring melatonin levels in CFS. I came to the conclusion

that there is not creased levels of melatonin in CFS. Who knows about

melatonin sensitivity though? I am not aware of any research measuring

SAMe levels or trialling SAMe supplements in CFS.

An extremely common cause of tryptophan depletion is bacterial imbalance

of the gut, converting tryptophan in other metabolites. Interestingly

bacterial overgrowth/imbalance is present in the vast majority of those

with CFS, as is depressed blood tryptophan levels.

There are dozens of inter-relating factors in insomnia. Many of these

are listed at my page on this topic:

http://www.nutritional-healing.com.au/content/condition.php?category=physical & co\

ndition=Insomnia

<http://www.nutritional-healing.com.au/content/condition.php?category=physical & c\

ondition=Insomnia>

Best regards, Blake Graham