Re: Update on Coagulation testing & Dr. Glueck.

[Guest guest]

Penny,

Coincidently, I was doing some research about Chlamydia pneumonia and its relevance to atherosclerosis and I was reading through this article when I read your post. You should find it interesting reading!

Nelly

http://www.jstage.jst.go.jp/article/circj/71/9/1480/_pdf

Discussion

Previous studies from our laboratory have shown that

chronic C. pneumoniae infection of apoE-KO mice may

cause injury to the aortic endothelium, as indicated by the

impaired aortic relaxation responses to the muscarinic

agonist methacholine (Fig 3). In the same animal model,

infection with C. pneumoniae caused lipid accumulation

and inflammatory changes in the aorta wall.

Using additional segments from the aortas previously

tested with methacholine, the findings of the present study

indicate that the responses to bradykinin are not altered in

the early phase of chronic infection with C. pneumoniae.

Moreover, the augmented relaxation responses to bradykinin

in the later stages of infection suggest that active regulatory

mechanisms in response to bradykinin stimulation could be

responsible for the observed differences. Although pretreatment

with the bradykinin B2-receptor antagonist Hoe140

abolished the relaxation response to bradykinin in infected

animals, the contribution of vascular endothelial kinin B1

receptors, which may be upregulated by infections and inflammation,

21 might be among the underlying mechanisms.

Earlier studies on vascular physiology in relation to

various risk factors for atherosclerosis have suggested a discrepancy

between the vasomotor responses to muscarinic

agonists and those elicited by bradykinin. Indeed, in the

majority of studies, impaired arterial vasomotor responses

to muscarinic receptor stimulation were documented,

whereas the responses to bradykinin were shown to be

preserved11–13 or even enhanced.14 It has therefore been

speculated that the endothelial injury in atherosclerosis is

receptor-specific, being confined at least in the early stages

to muscarinic receptors. The mechanisms proposed to explain

these findings have primarily depicted 2 possible

scenarios: either the kinin receptor pathway is spared in the

early stages, or regulatory kinin-mediated, endotheliumdependent

mechanisms are set in response to the injurious

stimuli. Such mechanisms might involve kinin-mediated

upregulation of endothelial pathways such as increased

synthesis of cyclooxygenase (COX)-dependent relaxant

prostaglandins.22

Although the arterial relaxation responses to methacholine

are largely mediated by NO, the relaxation to

bradykinin might in part involve both NO and prostacyclin,

a COX product with dilatory properties.16 However, in the

present study, blocking of either NO synthesis or COX

activity by L-NAME and diclofenac, respectively, did not

have a consistent inhibitory effect on the bradykinininduced

relaxation in the noninfected apoE-KO mice. This

suggests that at least in this animal model a non-NO, nonprostanoid

factor, possibly endothelial-derived hyperpolarizing

factor, is mainly responsible for the relaxant effects of

bradykinin. In contrast, pretreatment of aortas from infected

animals with L-NAME or diclofenac inhibited the relaxation

responses to bradykinin, suggesting that increased

production of both NO and relaxing prostaglandins, most

likely prostacyclin, are responsible for the augmented

relaxation to bradykinin in the infected animals. Because

the amounts of the COX and NOS enzyme proteins did not

differ between infected and noninfected animals,10 it is possible

that the activity of both the NOS and COX pathways

could have been upregulated by bradykinin in infected

animals, with a composite result of increased availability of

NO and relaxing prostaglandins.

Bradykinin could improve the bioactivity of NO by

serving as a substrate to NOS because of the L-arginine

incorporated in its structure,23 and by its interaction with

tetrahydrobiopterin,24 the coenzyme implicated in the NO

synthesis. This results in a better coupling of L-arginine and

NADPH oxidation, leading to improved bioactivity of NO.

These bradykinin-induced mechanisms may be important

in the setting of vascular pathologies, including atherosclerosis,

in which the levels of both L-arginine and tetrahydropterin

are suboptimal.25,26 Of note, L-arginine was

shown to improve the coronary reactivity in swine with C.

pneumoniae infection following repeated inoculations with

this pathogen,27 a finding that supports the hypothesis that

decreased availability of endothelial L-arginine could be

associated with this infection. The improvement in the NOS

pathway by bradykinin could in turn influence the COX

pathway, probably in part through a complex cross-talk between

the NOS and COX enzymes,28 with a subsequent

increase in the release of relaxant prostaglandin.

Under normal circumstances, bradykinin contributes to

regulation of both the resting tone and flow-mediated

dilatation of arteries, and exerts important antiatherogenic

effects through NO and prostacyclin.29,30 Of note, angiotensin-

converting enzyme (ACE) inhibitors improve vascular

endothelial function in various pathological conditions

associated with atherosclerosis, in part through increased

availability of bradykinin.31,32 Accumulating data from both

experimental studies and clinical trials suggest that ACE

inhibitors may retard the development of atherosclerosis

and its manifestations.18,33,34 Based on the present findings,

one might speculate that similar benefit could be attained

by ACE inhibitors on C. pneumoniae-induced endothelial

dysfunction and, perhaps, on the development of atherosclerosis

with an infectious basis.

In conclusion, bradykinin stimulation of the endothelium

of aortas from C. pneumoniae-infected apoE-KO animals

appears to activate compensatory kinin receptor-related

mechanisms that could involve NO and vasorelaxing prostanoids.

Additional studies are needed to further investigate

the molecular pathways, and, in particular, to verify whether

similar effects may occur in other animal models

[infections] Update on Coagulation testing & Dr. Glueck.

Hi all,

The status report on my coagulation testing is still in progress, although I do have some pretty significant news on how it's perhaps impacting my health so far.

Dr. Glueck has asked that I have 3 more tests performed before advising me on a full course of treatment (and remarkably, he's refusing any payment for his consultation, even though he's more than entitled). In the meantime, based on my medical history, he's telling me that testing positive for the ENOS (endothelial nitric oxide synthesis) mutation could be significant and problematic and he's advised that I start immediately taking an OTC medical food product called Arginaid. This is often used in the hospital setting for wound healing, diabetic ulcerations, etc. It's also used to prevent blood vessel and cornary spasming and reduce the risk of plaque build-up and heart attack. (people with this mutation have a 3-fold greater risk of heart attack).

Arginaid is a drink version of L-arginine, an essential amino acid which is a protein and Nitric Oxide precursor. Apparently, the ENOS defect makes it difficult to produce/synthesize Nitric Oxide, which is important for wound healing, fighting infection, muscle and vascular health, hormone production, etc. (Body builders commonly supplement with Arginine.) It's also good to note that infection depletes arginine stores. One of the known effects of poor Nitric Oxide synthesis is blood vessel spasming. This is extremely interesting to me personally because vessel spasms are thought to be at the root of migraines, something I've had to deal with for 2 decades. Doing more research on NO and arginine, I've just now learned that arginine is one of the supplements suggested in migraine treatment. So it looks as if things are perhaps coming full circle here. It's very possible that this coagulation defect is at the basis of my chronic infections, migraines, fatigue and overall pain and weakness.

With all the supplements I've taken, I've never taken Arginine. I've thought about taking it before, but based on the tremendous amount of supplement info out there and my lack of success with so many previous supplements, it's hard to know what's actually worth trying.

Having these test results pointing me in a specific & logical direction, however, gives me so much more confidence in how to approach my illness in general. Although I'm not convinced Arginine is the answer, knowing that my efforts are based on something concrete gives me a greater feeling of empowerment as well as more reasonable hope for some kind of success.

I still think it would be smart for all pwc, and pw/FMS to have coagulation testing done, but if that's not immediately possible, then I think that it would behoove pwc with symptoms similar to mine (and I know there are a lot of us out there) to do some research on Nitric Oxide synthesis and talk to their doctors about doing a therapeutic trial with arginine and see if some of their symptoms are alleviated. In the meantime, I will keep everyone posted on my trial with arginaid (as soon as it arrives), and will also update you once I've had the additional blood testing and get Dr. Glueck's full recommendations.

I have to say that I am more convinced than ever that Dr. Glueck is a very fine doctor, in addition to being a well known researcher and director of the Jewish Hospital in Cincinatti. He obviously cares about patients or he wouldn't be consulting people at no charge and continuously running free health studies for patients. His research has created a number of medical breakthroughs, resulting in better lives for so many people. I hope that his efforts will help pwc as well.

penny

Wikipedia on Nitric Oxide:

Arginine plays an important role in cell division, the healing of wounds, removing ammonia from the body, immune function, and the release of hormones. Arginine, taken in combination with proanthocyanidins[4] or yohimbine[5], has also been used as a treatment for erectile dysfunction.

In proteins

The geometry, charge distribution and ability to form multiple H-bonds make arginine ideal for binding negatively charged groups. For this reason arginine prefers to be on the outside of the proteins where it can interact with the polar environment. Incorporated in proteins, arginine can also be converted to citrulline by PAD enzymes. In addition, arginine can be methylated by protein methyltransferases.

As a precursor

Arginine is the immediate precursor of NO, urea, ornithine and agmatine; is necessary for the synthesis of creatine; and can also be used for the synthesis of polyamines (mainly through ornithine and to a lesser degree through agmatine), citrulline, and glutamate. For being a precursor of NO, (relaxes blood vessels), arginine is used in many conditions where vasodilation is required. The presence of asymmetric dimethylarginine (ADMA), a close relative, inhibits the nitric oxide reaction; therefore, ADMA is considered a marker for vascular disease, just as L-arginine is considered a sign of a healthy endothelium.

[Guest guest]

you might want to run this all on  cpnhelp.orgOn 16 Nov 2007, at 20:29, Nelly Pointis wrote:Penny, Coincidently, I was doing some research about Chlamydia pneumonia and its relevance to atherosclerosis and I was reading through this article when I read your post. You should find it interesting reading! Nelly  http://www.jstage.jst.go.jp/article/circj/71/9/1480/_pdfDiscussionPrevious studies from our laboratory have shown thatchronic C. pneumoniae infection of apoE-KO mice maycause injury to the aortic endothelium, as indicated by theimpaired aortic relaxation responses to the muscarinicagonist methacholine (Fig 3). In the same animal model,infection with C. pneumoniae caused lipid accumulationand inflammatory changes in the aorta wall.Using additional segments from the aortas previouslytested with methacholine, the findings of the present studyindicate that the responses to bradykinin are not altered inthe early phase of chronic infection with C. pneumoniae.Moreover, the augmented relaxation responses to bradykininin the later stages of infection suggest that active regulatorymechanisms in response to bradykinin stimulation could beresponsible for the observed differences. Although pretreatmentwith the bradykinin B2-receptor antagonist Hoe140abolished the relaxation response to bradykinin in infectedanimals, the contribution of vascular endothelial kinin B1receptors, which may be upregulated by infections and inflammation,21 might be among the underlying mechanisms.Earlier studies on vascular physiology in relation tovarious risk factors for atherosclerosis have suggested a discrepancybetween the vasomotor responses to muscarinicagonists and those elicited by bradykinin. Indeed, in themajority of studies, impaired arterial vasomotor responsesto muscarinic receptor stimulation were documented,whereas the responses to bradykinin were shown to bepreserved11–13 or even enhanced.14 It has therefore beenspeculated that the endothelial injury in atherosclerosis isreceptor-specific, being confined at least in the early stagesto muscarinic receptors. The mechanisms proposed to explainthese findings have primarily depicted 2 possiblescenarios: either the kinin receptor pathway is spared in theearly stages, or regulatory kinin-mediated, endotheliumdependentmechanisms are set in response to the injuriousstimuli. Such mechanisms might involve kinin-mediatedupregulation of endothelial pathways such as increasedsynthesis of cyclooxygenase (COX)-dependent relaxantprostaglandins.22Although the arterial relaxation responses to methacholineare largely mediated by NO, the relaxation tobradykinin might in part involve both NO and prostacyclin,a COX product with dilatory properties.16 However, in thepresent study, blocking of either NO synthesis or COXactivity by L-NAME and diclofenac, respectively, did nothave a consistent inhibitory effect on the bradykinininducedrelaxation in the noninfected apoE-KO mice. Thissuggests that at least in this animal model a non-NO, nonprostanoidfactor, possibly endothelial-derived hyperpolarizingfactor, is mainly responsible for the relaxant effects ofbradykinin. In contrast, pretreatment of aortas from infectedanimals with L-NAME or diclofenac inhibited the relaxationresponses to bradykinin, suggesting that increasedproduction of both NO and relaxing prostaglandins, mostlikely prostacyclin, are responsible for the augmentedrelaxation to bradykinin in the infected animals. Becausethe amounts of the COX and NOS enzyme proteins did notdiffer between infected and noninfected animals,10 it is possiblethat the activity of both the NOS and COX pathwayscould have been upregulated by bradykinin in infectedanimals, with a composite result of increased availability ofNO and relaxing prostaglandins.Bradykinin could improve the bioactivity of NO byserving as a substrate to NOS because of the L-arginineincorporated in its structure,23 and by its interaction withtetrahydrobiopterin,24 the coenzyme implicated in the NOsynthesis. This results in a better coupling of L-arginine andNADPH oxidation, leading to improved bioactivity of NO.These bradykinin-induced mechanisms may be importantin the setting of vascular pathologies, including atherosclerosis,in which the levels of both L-arginine and tetrahydropterinare suboptimal.25,26 Of note, L-arginine wasshown to improve the coronary reactivity in swine with C.pneumoniae infection following repeated inoculations withthis pathogen,27 a finding that supports the hypothesis thatdecreased availability of endothelial L-arginine could beassociated with this infection. The improvement in the NOSpathway by bradykinin could in turn influence the COXpathway, probably in part through a complex cross-talk betweenthe NOS and COX enzymes,28 with a subsequentincrease in the release of relaxant prostaglandin.Under normal circumstances, bradykinin contributes toregulation of both the resting tone and flow-mediateddilatation of arteries, and exerts important antiatherogeniceffects through NO and prostacyclin.29,30 Of note, angiotensin-converting enzyme (ACE) inhibitors improve vascularendothelial function in various pathological conditionsassociated with atherosclerosis, in part through increasedavailability of bradykinin.31,32 Accumulating data from bothexperimental studies and clinical trials suggest that ACEinhibitors may retard the development of atherosclerosisand its manifestations.18,33,34 Based on the present findings,one might speculate that similar benefit could be attainedby ACE inhibitors on C. pneumoniae-induced endothelialdysfunction and, perhaps, on the development of atherosclerosiswith an infectious basis.In conclusion, bradykinin stimulation of the endotheliumof aortas from C. pneumoniae-infected apoE-KO animalsappears to activate compensatory kinin receptor-relatedmechanisms that could involve NO and vasorelaxing prostanoids.Additional studies are needed to further investigatethe molecular pathways, and, in particular, to verify whethersimilar effects may occur in other animal models [infections] Update on Coagulation testing & Dr. Glueck.Hi all, The status report on my coagulation testing is still in progress, although I do have some pretty significant news on how it's perhaps impacting my health so far. Dr. Glueck has asked that I have 3 more tests performed before advising me on a full course of treatment (and remarkably, he's refusing any payment for his consultation, even though he's more than entitled). In the meantime, based on my medical history, he's telling me that testing positive for the ENOS (endothelial nitric oxide synthesis) mutation could be significant and problematic and he's advised that I start immediately taking an OTC medical food product called Arginaid. This is often used in the hospital setting for wound healing, diabetic ulcerations, etc. It's also used to prevent blood vessel and cornary spasming and reduce the risk of plaque build-up and heart attack. (people with this mutation have a 3-fold greater risk of heart attack). Arginaid is a drink version of L-arginine, an essential amino acid which is a protein and Nitric Oxide precursor. Apparently, the ENOS defect makes it difficult to produce/synthesize Nitric Oxide, which is important for wound healing, fighting infection, muscle and vascular health, hormone production, etc. (Body builders commonly supplement with Arginine.) It's also good to note that infection depletes arginine stores. One of the known effects of poor Nitric Oxide synthesis is blood vessel spasming. This is extremely interesting to me personally because vessel spasms are thought to be at the root of migraines, something I've had to deal with for 2 decades. Doing more research on NO and arginine, I've just now learned that arginine is one of the supplements suggested in migraine treatment. So it looks as if things are perhaps coming full circle here. It's very possible that this coagulation defect is at the basis of my chronic infections, migraines, fatigue and overall pain and weakness.With all the supplements I've taken, I've never taken Arginine. I've thought about taking it before, but based on the tremendous amount of supplement info out there and my lack of success with so many previous supplements, it's hard to know what's actually worth trying.Having these test results pointing me in a specific & logical direction, however, gives me so much more confidence in how to approach my illness in general. Although I'm not convinced Arginine is the answer, knowing that my efforts are based on something concrete gives me a greater feeling of empowerment as well as more reasonable hope for some kind of success. I still think it would be smart for all pwc, and pw/FMS to have coagulation testing done, but if that's not immediately possible, then I think  that it would behoove pwc with symptoms similar to mine (and I know there are a lot of us out there) to do some research on Nitric Oxide synthesis and talk to their doctors about doing a therapeutic trial with arginine and see if some of their symptoms are alleviated.  In the meantime, I will keep everyone posted on my trial with arginaid (as soon as it arrives), and will also update you once I've had the additional blood testing and get Dr. Glueck's full recommendations. I have to say that I am more convinced than ever that Dr. Glueck is a very fine doctor, in addition to being a well known researcher and director of the Jewish Hospital in Cincinatti. He obviously cares about patients or he wouldn't be consulting people at no charge and continuously running free health studies for patients. His research has created a number of medical breakthroughs, resulting in better lives for so many people. I hope that his efforts will help pwc as well. penny   Wikipedia on Nitric Oxide: Arginine plays an important role in cell division, the healing of wounds, removing ammonia from the body, immune function, and the release of hormones. Arginine, taken in combination with proanthocyanidins[4] or yohimbine[5], has also been used as a treatment for erectile dysfunction.In proteinsThe geometry, charge distribution and ability to form multiple H-bonds make arginine ideal for binding negatively charged groups. For this reason arginine prefers to be on the outside of the proteins where it can interact with the polar environment. Incorporated in proteins, arginine can also be converted to citrulline by PAD enzymes. In addition, arginine can be methylated by protein methyltransferases.As a precursorArginine is the immediate precursor of NO, urea, ornithine and agmatine; is necessary for the synthesis of creatine; and can also be used for the synthesis of polyamines (mainly through ornithine and to a lesser degree through agmatine), citrulline, and glutamate. For being a precursor of NO, (relaxes blood vessels), arginine is used in many conditions where vasodilation is required. The presence ofasymmetric dimethylarginine (ADMA), a close relative, inhibits the nitric oxide reaction; therefore, ADMA is considered a marker for vascular disease, just as L-arginine is considered a sign of a healthy endothelium.

[Guest guest]

There's HEAPS of stuff on atherosclerosis and chlamydia pneumoniae, I wouldn't know what to start bringing up, I suspect somebody like Dr Wheldon knows of all the research that keeps being produced.

Nelly

[infections] Update on Coagulation testing & Dr. Glueck.

Hi all,

The status report on my coagulation testing is still in progress, although I do have some pretty significant news on how it's perhaps impacting my health so far.

Dr. Glueck has asked that I have 3 more tests performed before advising me on a full course of treatment (and remarkably, he's refusing any payment for his consultation, even though he's more than entitled). In the meantime, based on my medical history, he's telling me that testing positive for the ENOS (endothelial nitric oxide synthesis) mutation could be significant and problematic and he's advised that I start immediately taking an OTC medical food product called Arginaid. This is often used in the hospital setting for wound healing, diabetic ulcerations, etc. It's also used to prevent blood vessel and cornary spasming and reduce the risk of plaque build-up and heart attack. (people with this mutation have a 3-fold greater risk of heart attack).

Arginaid is a drink version of L-arginine, an essential amino acid which is a protein and Nitric Oxide precursor. Apparently, the ENOS defect makes it difficult to produce/synthesize Nitric Oxide, which is important for wound healing, fighting infection, muscle and vascular health, hormone production, etc. (Body builders commonly supplement with Arginine.) It's also good to note that infection depletes arginine stores. One of the known effects of poor Nitric Oxide synthesis is blood vessel spasming. This is extremely interesting to me personally because vessel spasms are thought to be at the root of migraines, something I've had to deal with for 2 decades. Doing more research on NO and arginine, I've just now learned that arginine is one of the supplements suggested in migraine treatment. So it looks as if things are perhaps coming full circle here. It's very possible that this coagulation defect is at the basis of my chronic infections, migraines, fatigue and overall pain and weakness.

With all the supplements I've taken, I've never taken Arginine. I've thought about taking it before, but based on the tremendous amount of supplement info out there and my lack of success with so many previous supplements, it's hard to know what's actually worth trying.

Having these test results pointing me in a specific & logical direction, however, gives me so much more confidence in how to approach my illness in general. Although I'm not convinced Arginine is the answer, knowing that my efforts are based on something concrete gives me a greater feeling of empowerment as well as more reasonable hope for some kind of success.

I still think it would be smart for all pwc, and pw/FMS to have coagulation testing done, but if that's not immediately possible, then I think that it would behoove pwc with symptoms similar to mine (and I know there are a lot of us out there) to do some research on Nitric Oxide synthesis and talk to their doctors about doing a therapeutic trial with arginine and see if some of their symptoms are alleviated. In the meantime, I will keep everyone posted on my trial with arginaid (as soon as it arrives), and will also update you once I've had the additional blood testing and get Dr. Glueck's full recommendations.

I have to say that I am more convinced than ever that Dr. Glueck is a very fine doctor, in addition to being a well known researcher and director of the Jewish Hospital in Cincinatti. He obviously cares about patients or he wouldn't be consulting people at no charge and continuously running free health studies for patients. His research has created a number of medical breakthroughs, resulting in better lives for so many people. I hope that his efforts will help pwc as well.

penny

Wikipedia on Nitric Oxide:

Arginine plays an important role in cell division, the healing of wounds, removing ammonia from the body, immune function, and the release of hormones. Arginine, taken in combination with proanthocyanidins[4] or yohimbine[5], has also been used as a treatment for erectile dysfunction.

In proteins

The geometry, charge distribution and ability to form multiple H-bonds make arginine ideal for binding negatively charged groups. For this reason arginine prefers to be on the outside of the proteins where it can interact with the polar environment. Incorporated in proteins, arginine can also be converted to citrulline by PAD enzymes. In addition, arginine can be methylated by protein methyltransferases.

As a precursor

Arginine is the immediate precursor of NO, urea, ornithine and agmatine; is necessary for the synthesis of creatine; and can also be used for the synthesis of polyamines (mainly through ornithine and to a lesser degree through agmatine), citrulline, and glutamate. For being a precursor of NO, (relaxes blood vessels), arginine is used in many conditions where vasodilation is required. The presence ofasymmetric dimethylarginine (ADMA), a close relative, inhibits the nitric oxide reaction; therefore, ADMA is considered a marker for vascular disease, just as L-arginine is considered a sign of a healthy endothelium.

[Guest guest]

I have a Chronic Fatigue friend that attributes her very good

improvements to Dr. Glueck.

I'm glad he sounds like a Doc that really wants his patients to

improve their quality of life while actually rying to find out why

they feel the way they do. That's a rarity.

You know the old saying You are What You Eat.

I also have a friend with interstitial cystitis (chronic infection if

the lining of the bladder) who can control it with diet (keeping the

urine more alkaline) - and this after thousands of $$- antibiotics

(which can't get this bug apparently burried in the bladder lining)

and invasive procedures.

Keep us posted..

Barb

>

> Hi all,

>

> The status report on my coagulation testing is still in progress,

although I do have some pretty significant news on how it's perhaps

impacting my health so far.

>

> Dr. Glueck has asked that I have 3 more tests performed before

advising me on a full course of treatment (and remarkably, he's

refusing any payment for his consultation, even though he's more than

entitled). In the meantime, based on my medical history, he's telling

me that testing positive for the ENOS (endothelial nitric oxide

synthesis) mutation could be significant and problematic and he's

advised that I start immediately taking an OTC medical food product

called Arginaid. This is often used in the hospital setting for wound

healing, diabetic ulcerations, etc. It's also used to prevent blood

vessel and cornary spasming and reduce the risk of plaque build-up

and heart attack. (people with this mutation have a 3-fold greater

risk of heart attack).

>

> Arginaid is a drink version of L-arginine, an essential amino

acid which is a protein and Nitric Oxide precursor. Apparently, the

ENOS defect makes it difficult to produce/synthesize Nitric Oxide,

which is important for wound healing, fighting infection, muscle and

vascular health, hormone production, etc. (Body builders commonly

supplement with Arginine.) It's also good to note that infection

depletes arginine stores. One of the known effects of poor Nitric

Oxide synthesis is blood vessel spasming. This is extremely

interesting to me personally because vessel spasms are thought to be

at the root of migraines, something I've had to deal with for 2

decades. Doing more research on NO and arginine, I've just now

learned that arginine is one of the supplements suggested in migraine

treatment. So it looks as if things are perhaps coming full circle

here. It's very possible that this coagulation defect is at the basis

of my chronic infections, migraines, fatigue and overall

> pain and weakness.

>

> With all the supplements I've taken, I've never taken Arginine.

I've thought about taking it before, but based on the tremendous

amount of supplement info out there and my lack of success with so

many previous supplements, it's hard to know what's actually worth

trying.

> Having these test results pointing me in a specific & logical

direction, however, gives me so much more confidence in how to

approach my illness in general. Although I'm not convinced Arginine

is the answer, knowing that my efforts are based on something

concrete gives me a greater feeling of empowerment as well as more

reasonable hope for some kind of success.

>

> I still think it would be smart for all pwc, and pw/FMS to have

coagulation testing done, but if that's not immediately possible,

then I think that it would behoove pwc with symptoms similar to mine

(and I know there are a lot of us out there) to do some research on

Nitric Oxide synthesis and talk to their doctors about doing a

therapeutic trial with arginine and see if some of their symptoms are

alleviated. In the meantime, I will keep everyone posted on my trial

with arginaid (as soon as it arrives), and will also update you once

I've had the additional blood testing and get Dr. Glueck's full

recommendations.

>

> I have to say that I am more convinced than ever that Dr. Glueck

is a very fine doctor, in addition to being a well known researcher

and director of the Jewish Hospital in Cincinatti. He obviously cares

about patients or he wouldn't be consulting people at no charge and

continuously running free health studies for patients. His research

has created a number of medical breakthroughs, resulting in better

lives for so many people. I hope that his efforts will help pwc as

well.

>

> penny

>

>

>

> Wikipedia on Nitric Oxide:

>

> Arginine plays an important role in cell division, the healing of

wounds, removing ammonia from the body, immune function, and the

release of hormones. Arginine, taken in combination with

proanthocyanidins[4] or yohimbine[5], has also been used as a

treatment for erectile dysfunction.

>

> In proteins The geometry, charge distribution and ability to

form multiple H-bonds make arginine ideal for binding negatively

charged groups. For this reason arginine prefers to be on the outside

of the proteins where it can interact with the polar environment.

Incorporated in proteins, arginine can also be converted to

citrulline by PAD enzymes. In addition, arginine can be methylated by

protein methyltransferases.

>

> As a precursor Arginine is the immediate precursor of NO, urea,

ornithine and agmatine; is necessary for the synthesis of creatine;

and can also be used for the synthesis of polyamines (mainly through

ornithine and to a lesser degree through agmatine), citrulline, and

glutamate. For being a precursor of NO, (relaxes blood vessels),

arginine is used in many conditions where vasodilation is required.

The presence of asymmetric dimethylarginine (ADMA), a close relative,

inhibits the nitric oxide reaction; therefore, ADMA is considered a

marker for vascular disease, just as L-arginine is considered a sign

of a healthy endothelium.

>