Re: Failed AVS Redux

[Guest guest]

My AVS result is posted at http://f1.grp.yahoofs.com/v1/oA0FTUxifmQwNxLXlhYEs5coop5S9LWOlpHBaGKMb6QnvxzPs6mgwM5DBr-SJunvsrIN4FFp0h5P3VrcKk-xgnKnWWxY/AVS%20Experiences/avs.jpg

Subject: Failed AVS ReduxTo: "Aldo Hyper" <hyperaldosteronism >Date: Sunday, December 12, 2010, 1:37 PM

A month or two back, I posted numbers from my AVS. Fortunately Dr Grim recognized they showed a failure. To satisfy my endo, I got third opinion from another expert, this one also a nationally recognized authority like Dr Grim. For the time being, my endo has fired me, but I anticipate that might change. He's a good man and a good doc in a confusing situation and probably experience pressures from above and around to join a wall of silence and denial.

http://hyperaldo-too.blogspot.com/2010/12/report-from-my-avs.html

I have gone looking for other AVS reports on the web with little success, so I have two questions:

1) Is there a place where I can see two dozen or more AVS reports on the web?

2) From the few AVS reports I HAVE found, I gather that my cortisol numbers are 1/10 or 1/20 of the ballpark one would expect under ACTH stimulation. (Dr Grim noted earlier there must have been some problem with the ACTH stimulation.) I was also on 100 mg (half my usual dose) of eplerenone.

But just suppose there was no glitch in administering the ACTH. Does this suggest an inhibition or deficiency in the enzyme P450-17alpha, the enzyme #3 that "passes along" hormones from "pathway 1" to "pathway 2" in the diagram here:

http://www.dshs.state.tx.us/newborn/prenatal.shtm

I link the article for the relevance of the diagram, not the relevance of the article, which seems (on superficial examination) to examine some other deficiency.

The secondary sex characteristics are mildly attenuated in males in my family, and those characteristics come from pathway 3. If it is hard to reach pathway 2, then it is also hard to reach pathway 3.

If raw materials cannot get passed from pathway 1 to pathway 2, then the patient ends up with too much aldosterone, is that correct?

Is P450-17alpha inhibition or deficiency one of the recognized familial problems? (Is it GRA?) Are other causes of it known? Even if not, is it recognized as a distinctive mechanism of hyperaldosteronism? Is there a specialized treatment for it?

Thanks for any and all perspective,

AG

[Guest guest]

Thanks for providing that link, a.

Now that I've looked a little farther, I see that this enzyme is called 17-hydroxylase and a deficiency can indeed be hereditary and it is one of the rarer recognized forms of congenital adrenal hyperplasia. In classic form, it produces early and severe disruption of sexual development.

(If I didn't have so much brain fog, I would remember these things from earlier investigation. I used to be brilliant that way, but no longer.)

However, it apparently occurs in many degrees of severity.

And that is apparently the enzyme also discussed by Marcia Ruth Roper in her book about which I posted some weeks back, " Type 2 Diabetes: The Adrenal Disease. " Recall that she works with the Native American population and claims that a hereditary disruption in this enzyme is the root of their hereditary predisposition toward Type 2 diabetes and, according to Roper, the cause of their high sensitivity to caffeine as a disruptor of blood sugar metabolism.

In her population, the bottleneck is between Pathway 2 and Pathway 3. (See my earlier post.) In my, hypothetically, the bottleneck would be between Pathway 1 and Pathway 2. Otherwise, the mechanism of native American diabetes is the same as the mechanism of primary aldosteronism caused by 17-hydroxylase deficiency or inhibition. (Roper claims caffeine is an inhibitor.)

So I guess the question becomes, could my low cortisol under ACTH stimulation equally well indicate some degree of 17-hydroxylase deficiency and a mild form of CAH? Or would that have been unmissably obvious from other symptoms or tests by now? And if so, would it respond to dexamethasone or some other treatment?

AG

A month or two back, I posted numbers from my AVS. Fortunately Dr Grim recognized they showed a failure. To satisfy my endo, I got third opinion from another expert, this one also a nationally recognized authority like Dr Grim. For the time being, my endo has fired me, but I anticipate that might change. He's a good man and a good doc in a confusing situation and probably experience pressures from above and around to join a wall of silence and denial.

http://hyperaldo-too.blogspot.com/2010/12/report-from-my-avs.html

etc...

[Guest guest]

a, I can hardly believe how much more professional-looking your report is than mine. Or actually, I should say that the other way. I can't believe how unprofessional the report I received looks compared to yours. Especially for a $13,000 procedure. It also appears your test itself was much more thorough than mine.

It just reinforces all those old (and in my opinion unjustified today) stereotypes about the South.

My AVS result is posted at http://f1.grp.yahoofs.com/v1/oA0FTUxifmQwNxLXlhYEs5coop5S9LWOlpHBaGKMb6QnvxzPs6mgwM5DBr-SJunvsrIN4FFp0h5P3VrcKk-xgnKnWWxY/AVS%20Experiences/avs.jpg

[Guest guest]

Is it also in our data base? I am not sure we have a place to put it as I recall. Any suggestions for the abstract? I can revise it I will be trying to update it later today.When I clicked on your link a I got the message not found.CEMy AVS result is posted at http://f1.grp.yahoofs.com/v1/oA0FTUxifmQwNxLXlhYEs5coop5S9LWOlpHBaGKMb6QnvxzPs6mgwM5DBr-SJunvsrIN4FFp0h5P3VrcKk-xgnKnWWxY/AVS%20Experiences/avs.jpg --- Subject: Failed AVS ReduxTo: "Aldo Hyper" <hyperaldosteronism >Date: Sunday, December 12, 2010, 1:37 PM A month or two back, I posted numbers from my AVS. Fortunately Dr Grim recognized they showed a failure. To satisfy my endo, I got third opinion from another expert, this one also a nationally recognized authority like Dr Grim. For the time being, my endo has fired me, but I anticipate that might change. He's a good man and a good doc in a confusing situation and probably experience pressures from above and around to join a wall of silence and denial. http://hyperaldo-too.blogspot.com/2010/12/report-from-my-avs.html I have gone looking for other AVS reports on the web with little success, so I have two questions: 1) Is there a place where I can see two dozen or more AVS reports on the web? 2) From the few AVS reports I HAVE found, I gather that my cortisol numbers are 1/10 or 1/20 of the ballpark one would expect under ACTH stimulation. (Dr Grim noted earlier there must have been some problem with the ACTH stimulation.) I was also on 100 mg (half my usual dose) of eplerenone. But just suppose there was no glitch in administering the ACTH. Does this suggest an inhibition or deficiency in the enzyme P450-17alpha, the enzyme #3 that "passes along" hormones from "pathway 1" to "pathway 2" in the diagram here: http://www.dshs.state.tx.us/newborn/prenatal.shtm I link the article for the relevance of the diagram, not the relevance of the article, which seems (on superficial examination) to examine some other deficiency. The secondary sex characteristics are mildly attenuated in males in my family, and those characteristics come from pathway 3. If it is hard to reach pathway 2, then it is also hard to reach pathway 3. If raw materials cannot get passed from pathway 1 to pathway 2, then the patient ends up with too much aldosterone, is that correct? Is P450-17alpha inhibition or deficiency one of the recognized familial problems? (Is it GRA?) Are other causes of it known? Even if not, is it recognized as a distinctive mechanism of hyperaldosteronism? Is there a specialized treatment for it? Thanks for any and all perspective,AG

[Guest guest]

Welcome to the club of

" fired but still sick people. "

They always fire you if they can't figure you out or if you are too well

informed. I fired one after

witnessing that he was a complete idiot.

Others, I've just not gone back to, but I do sometimes rate them on

various web sites.

Val

---

From: Alden alden.g@...

For the time being, my endo

has fired me, but I anticipate that might change. He's a good man and a

good doc in a confusing situation and probably experience pressures from

above and around to join a wall of silence and denial.

[Guest guest]

Yeah, it's in the files, Yahoo always messes up links for some reason. Click on files, then AVS experiences then avs.jpg a's AVS report. The abstract looked good to me.

a

Subject: Failed AVS ReduxTo: "Aldo Hyper" <hyperaldosteronism >Date: Sunday, December 12, 2010, 1:37 PM

A month or two back, I posted numbers from my AVS. Fortunately Dr Grim recognized they showed a failure. To satisfy my endo, I got third opinion from another expert, this one also a nationally recognized authority like Dr Grim. For the time being, my endo has fired me, but I anticipate that might change. He's a good man and a good doc in a confusing situation and probably experience pressures from above and around to join a wall of silence and denial.

http://hyperaldo-too.blogspot.com/2010/12/report-from-my-avs.html

I have gone looking for other AVS reports on the web with little success, so I have two questions:

1) Is there a place where I can see two dozen or more AVS reports on the web?

2) From the few AVS reports I HAVE found, I gather that my cortisol numbers are 1/10 or 1/20 of the ballpark one would expect under ACTH stimulation. (Dr Grim noted earlier there must have been some problem with the ACTH stimulation.) I was also on 100 mg (half my usual dose) of eplerenone.

But just suppose there was no glitch in administering the ACTH. Does this suggest an inhibition or deficiency in the enzyme P450-17alpha, the enzyme #3 that "passes along" hormones from "pathway 1" to "pathway 2" in the diagram here:

http://www.dshs.state.tx.us/newborn/prenatal.shtm

I link the article for the relevance of the diagram, not the relevance of the article, which seems (on superficial examination) to examine some other deficiency.

The secondary sex characteristics are mildly attenuated in males in my family, and those characteristics come from pathway 3. If it is hard to reach pathway 2, then it is also hard to reach pathway 3.

If raw materials cannot get passed from pathway 1 to pathway 2, then the patient ends up with too much aldosterone, is that correct?

Is P450-17alpha inhibition or deficiency one of the recognized familial problems? (Is it GRA?) Are other causes of it known? Even if not, is it recognized as a distinctive mechanism of hyperaldosteronism? Is there a specialized treatment for it?

Thanks for any and all perspective,

AG

[Guest guest]

A month or two back, I posted numbers from my AVS. Fortunately Dr Grim recognized they showed a failure. To satisfy my endo, I got third opinion from another expert, this one also a nationally recognized authority like Dr Grim. For the time being, my endo has fired me, but I anticipate that might change. He's a good man and a good doc in a confusing situation and probably experience pressures from above and around to join a wall of silence and denial. http://hyperaldo-too.blogspot.com/2010/12/report-from-my-avs.html I have gone looking for other AVS reports on the web with little success, so I have two questions: 1) Is there a place where I can see two dozen or more AVS reports on the web? 2) From the few AVS reports I HAVE found, I gather that my cortisol numbers are 1/10 or 1/20 of the ballpark one would expect under ACTH stimulation. (Dr Grim noted earlier there must have been some problem with the ACTH stimulation.) I was also on 100 mg (half my usual dose) of eplerenone. But just suppose there was no glitch in administering the ACTH. Does this suggest an inhibition or deficiency in the enzyme P450-17alpha, the enzyme #3 that "passes along" hormones from "pathway 1" to "pathway 2" in the diagram here: http://www.dshs.state.tx.us/newborn/prenatal.shtm I link the article for the relevance of the diagram, not the relevance of the article, which seems (on superficial examination) to examine some other deficiency. The secondary sex characteristics are mildly attenuated in males in my family, and those characteristics come from pathway 3. If it is hard to reach pathway 2, then it is also hard to reach pathway 3. If raw materials cannot get passed from pathway 1 to pathway 2, then the patient ends up with too much aldosterone, is that correct?Right. Is P450-17alpha inhibition or deficiency one of the recognized familial problems? (Is it GRA? ) No it is not GRA. Read my review again.Here is a better review on the whole picture.I recommend you get the AHA Hypertension Primer 4th edition as a good source of what every Dr should know about HTN when they graduate from medical school. I can assure you that most have never seen this book. We have the chap on BP measurement. Are other causes of it known? Even if not, is it recognized as a distinctive mechanism of hyperaldosteronism? Is there a specialized treatment for it? Thanks for any and all perspective,When one hears hoofbeats one should look for horses not zebras. So when I saw your numbers the first issue is you did get ACTH, you did not get enough or what you got was out of date. Should be easy to test if this is possible. Give ACTH and see if your peripheral cortisol goes up. Called an ACTH Stimulation test.I have a beer that it will be normal.AG

[Guest guest]

Wonder why I can't see it at the site.Be sure to post yours in our files as well if you have not.I should work on a standardized report form if we don't have one yet.a, I can hardly believe how much more professional-looking your report is than mine. Or actually, I should say that the other way. I can't believe how unprofessional the report I received looks compared to yours. Especially for a $13,000 procedure. It also appears your test itself was much more thorough than mine. It just reinforces all those old (and in my opinion unjustified today) stereotypes about the South. My AVS result is posted at http://f1.grp.yahoofs.com/v1/oA0FTUxifmQwNxLXlhYEs5coop5S9LWOlpHBaGKMb6QnvxzPs6mgwM5DBr-SJunvsrIN4FFp0h5P3VrcKk-xgnKnWWxY/AVS%20Experiences/avs.jpg

[Guest guest]

What are the options for filing complaints to the State Medical Board good old boys?CE Grim MDWelcome to the club of "fired but still sick people." They always fire you if they can't figure you out or if you are too well informed. I fired one after witnessing that he was a complete idiot. Others, I've just not gone back to, but I do sometimes rate them on various web sites. Val From: Alden alden.g@...For the time being, my endo has fired me, but I anticipate that might change. He's a good man and a good doc in a confusing situation and probably experience pressures from above and around to join a wall of silence and denial.

[Guest guest]

Do we have place for AVS in our data base. I don't think so. Can we add one after we think about it?Have you seen the new interactive CD we produced for the MI Health Dept to update staff on proper BP technique now that mercury is gone from MI? I think you can request it from the MI health dept. CE Clarence Grimlowerbp2@...Seasons Greetings and Yeah, it's in the files, Yahoo always messes up links for some reason. Click on files, then AVS experiences then avs.jpg a's AVS report. The abstract looked good to me. a Subject: Failed AVS ReduxTo: "Aldo Hyper" <hyperaldosteronism >Date: Sunday, December 12, 2010, 1:37 PM A month or two back, I posted numbers from my AVS. Fortunately Dr Grim recognized they showed a failure. To satisfy my endo, I got third opinion from another expert, this one also a nationally recognized authority like Dr Grim. For the time being, my endo has fired me, but I anticipate that might change. He's a good man and a good doc in a confusing situation and probably experience pressures from above and around to join a wall of silence and denial. http://hyperaldo-too.blogspot.com/2010/12/report-from-my-avs.html I have gone looking for other AVS reports on the web with little success, so I have two questions: 1) Is there a place where I can see two dozen or more AVS reports on the web? 2) From the few AVS reports I HAVE found, I gather that my cortisol numbers are 1/10 or 1/20 of the ballpark one would expect under ACTH stimulation. (Dr Grim noted earlier there must have been some problem with the ACTH stimulation.) I was also on 100 mg (half my usual dose) of eplerenone. But just suppose there was no glitch in administering the ACTH. Does this suggest an inhibition or deficiency in the enzyme P450-17alpha, the enzyme #3 that "passes along" hormones from "pathway 1" to "pathway 2" in the diagram here: http://www.dshs.state.tx.us/newborn/prenatal.shtm I link the article for the relevance of the diagram, not the relevance of the article, which seems (on superficial examination) to examine some other deficiency. The secondary sex characteristics are mildly attenuated in males in my family, and those characteristics come from pathway 3. If it is hard to reach pathway 2, then it is also hard to reach pathway 3. If raw materials cannot get passed from pathway 1 to pathway 2, then the patient ends up with too much aldosterone, is that correct? Is P450-17alpha inhibition or deficiency one of the recognized familial problems? (Is it GRA?) Are other causes of it known? Even if not, is it recognized as a distinctive mechanism of hyperaldosteronism? Is there a specialized treatment for it? Thanks for any and all perspective,AG

[Guest guest]

But suppose in addition that I have hypospadias. And my mother possibly also had hypospadias. Do you begin to see zebra-stripes off in the distance?

When one hears hoofbeats one should look for horses not zebras. So when I saw your numbers the first issue is you did get ACTH, you did not get enough or what you got was out of date.

Should be easy to te st if this is possible. Give ACTH and see if your peripheral cortisol goes up. Called an ACTH Stimulation test.

I have a beer that it will be normal.

[Guest guest]

It's on the survey-

18. Have you had AVS?

19. If yes to above:

-where was it done?

-done properly with ATCH?

-both sides sucessfully done?

And I noticed they have a new option, it will not let you update/change your answers. I changed the default setting to allow updates. If anybody wants to update their results they can do so at http://www.kwiksurveys.com/online-survey.php?surveyID=HIJIO_f2685379

a

Subject: Re: Failed AVS ReduxTo: hyperaldosteronism Cc: "Clarence Grim" Date: Sunday, December 12, 2010, 3:16 PM

Do we have place for AVS in our data base. I don't think so. Can we add one after we think about it?

Have you seen the new interactive CD we produced for the MI Health Dept to update staff on proper BP technique now that mercury is gone from MI? I think you can request it from the MI health dept.

[Guest guest]

You need another ACTH test with urines as well is my guess by someone who is expert in this. You want to establish the DX before RX.I forget where you are I might know someone. It is so rare that I have never seen one.Would be good to have in your intro a brief sketch of who you are so I can better keep track.My opinion is that the diabetes problem is from eating too much and not exercising enough mostly.But will try to review what she is saying. Does she have a web site.Of course PA and its early stages will also be associated with DM II as aldo increases insulin resisitance and low K impairs insulin release.The first pt had DM II that was cured for years but eventually returned as did HTN.CE Grim MDThanks for providing that link, a. Now that I've looked a little farther, I see that this enzyme is called 17-hydroxylase and a deficiency can indeed be hereditary and it is one of the rarer recognized forms of congenital adrenal hyperplasia. In classic form, it produces early and severe disruption of sexual development. (If I didn't have so much brain fog, I would remember these things from earlier investigation. I used to be brilliant that way, but no longer.) However, it apparently occurs in many degrees of severity. And that is apparently the enzyme also discussed by Marcia Ruth Roper in her book about which I posted some weeks back, "Type 2 Diabetes: The Adrenal Disease." Recall that she works with the Native American population and claims that a hereditary disruption in this enzyme is the root of their hereditary predisposition toward Type 2 diabetes and, according to Roper, the cause of their high sensitivity to caffeine as a disruptor of blood sugar metabolism. In her population, the bottleneck is between Pathway 2 and Pathway 3. (See my earlier post.) In my, hypothetically, the bottleneck would be between Pathway 1 and Pathway 2. Otherwise, the mechanism of native American diabetes is the same as the mechanism of primary aldosteronism caused by 17-hydroxylase deficiency or inhibition. (Roper claims caffeine is an inhibitor.) So I guess the question becomes, could my low cortisol under ACTH stimulation equally well indicate some degree of 17-hydroxylase deficiency and a mild form of CAH? Or would that have been unmissably obvious from other symptoms or tests by now? And if so, would it respond to dexamethasone or some other treatment? AG A month or two back, I posted numbers from my AVS. Fortunately Dr Grim recognized they showed a failure. To satisfy my endo, I got third opinion from another expert, this one also a nationally recognized authority like Dr Grim. For the time being, my endo has fired me, but I anticipate that might change. He's a good man and a good doc in a confusing situation and probably experience pressures from above and around to join a wall of silence and denial. http://hyperaldo-too.blogspot.com/2010/12/report-from-my-avs.html etc...

[Guest guest]

Ah but given that info I begin to think of a different type of horse. A physical exam would have also added that info if done carefully.Don't know the genetics of hypospadias. Did not even know women could get it. Always learning something.Did she take hormones when pregnant with you?http://www.cdc.gov/DES/consumers/research/recent_hypospadias.htmlOn Dec 12, 2010, at 1:21 PM, Alden wrote: But suppose in addition that I have hypospadias. And my mother possibly also had hypospadias. Do you begin to see zebra-stripes off in the distance? When one hears hoofbeats one should look for horses not zebras. So when I saw your numbers the first issue is you did get ACTH, you did not get enough or what you got was out of date. Should be easy to te st if this is possible. Give ACTH and see if your peripheral cortisol goes up. Called an ACTH Stimulation test. I have a beer that it will be normal.

[Guest guest]

I'm in Atlanta and I do not have diabetes. My a1c has always been acceptable.

I only mention the diabetes because Roper's book is where I first saw the diagram of adrenal hormone pathways and recognized that if Roper is correct, the difference between diabetes and hyperaldosteronism could be as small this single enzyme.

Marcia Ruth Roper's book is here:

http://books.google.com/books?id=NHom29q7jLsC & printsec=frontcover & dq=marcia+ruth+roper & source=bl & ots=BulZDWAFom & sig=ZqO-FPCXVxYf1Pdl2USNEqEyBfs & hl=en & ei=8DUFTbGUJoSclgfVorywBw & sa=X & oi=book_result & ct=result & resnum=1 & ved=0CBMQ6AEwAA#v=onepage & q & f=false

If the link doesn't work, it is titled " Type 2 Diabetes: The Adrenal Gland Disease " and there are many other sources for it. I linked this one because you may be able to read some of the book online at this link. I'm not sure.

I cannot find a website for Roper herself.

Apart from this claim about congenital 17-hydroxylase deficiency in the southwest Native American population and caffeine's inhibition of 17-hydroxylase in the Native American population, I do not think the book contains anything that would surprise you or most other competent endocrinologists. It is basic diabetes-for-the-patient stuff.

But come to think of it, her ideas about genetic adaption to heat in the southwest Native Americans may be related to your ideas about adaptation to heat in the African-American population. I don't know enough to be sure. But maybe you two would have some interesting discussions...

AG

You need another ACTH test with urines as well is my guess by someone who is expert in this. You want to establish the DX before RX.

I forget where you are I might know someone. It is so rare that I have never seen one.

Would be good to have in your intro a brief sketch of who you are so I can better keep track.

My opinion is that the diabetes problem is from eating too much and not exercising enough mostly.

But will try to review what she is saying. Does she have a web site.

Of course PA and its early stages will also be associated with DM II as aldo increases insulin resisitance and low K impairs insulin release.

The first pt had DM II that was cured for years but eventually returned as did HTN.

CE Grim MD

Thanks for providing that link, a.

Now that I've looked a little farther, I see that this enzyme is called 17-hydroxylase and a deficiency can indeed be hereditary and it is one of the rarer recognized forms of congenital adrenal hyperplasia. In classic form, it produces early and severe disruptio n of sexual development.

(If I didn't have so much brain fog, I would remember these things from earlier investigation. I used to be brilliant that way, but no longer.)

However, it apparently occurs in many degrees of severity.

And that is apparently the enzyme also discussed by Marcia Ruth Roper in her book about which I posted some weeks back, " Type 2 Diabetes: The Adrenal Disease. " Recall that she works with the Native American population and claims that a hereditary disruption in this enzyme is the root of their hereditary predisposition toward Type 2 diabetes and, according to Roper, the cause of their high sensitivity to caffeine as a disruptor of blood sugar metabolism.

In her population, the bottleneck is between Pathway 2 and Pathway 3. (See my earlier post.) In my, hypothetically, the bottleneck would be between Pathway 1 and Pathway 2 . Otherwise, the mechanism of native American diabetes is the same as the mechanism of primary aldosteronism caused by 17-hydroxylase deficiency or inhibition. (Roper claims caffeine is an inhibitor.)

So I guess the question becomes, could my low cortisol under ACTH stimulation equally well indicate some degree of 17-hydroxylase deficiency and a mild form of CAH? Or would that have been unmissably obvious from other symptoms or tests by now? And if so, would it respond to dexamethasone or some other treatment?

AG

A month or two back, I posted numbers from my AVS. Fortunately Dr Grim recognized they showed a failure. To satisfy my endo, I got third opinion from another expert, this one also a nationally recognized authority like Dr Grim. For the time being, my endo has fired me, but I anticipate that might change. He's a good man and a good doc in a confusing situation and probably experience pressures from above and around to join a wall of silence and denial.

http://hyperaldo-too.blogspot.com/2010/12/report-from-my-avs.html

etc...

[Guest guest]

I don't know if she took hormones. She died in 2001 and I am checking with my dad to find out whether it was the hypspadias or the vitiligo that we had in common. I know he said something long ago about her having my condition, too. Now the question is " which condition " -- vitiligo or hypospadias. I didn't even know myself that I had any abnormality until some offhand remark a PCP made during a physical when I was about 45. It's first-degree or even sub-first-degree but a urologist confirmed it is definitely hypospadias.

My PCP and endo both know very definitely about my hypospadias because I made a big deal about finding out whether or not I was going to have to have a urinary catheter for the AVS. But if there is some potential connection from the hypospadias to the hyperaldo, they have no clue about that. And in fairness, I wouldn't necessarily expect them to know something *that* esoteric, as long as they are open to finding out.

So what is the different kind of horse you are pondering?

AG

Ah but given that info I begin to think of a different type of horse. A physical exam would have also added that info if done carefully.

Don't know the genetics of hypospadias. Did not even know women could get it. Always learning something.

Did she take hormones when pregnant with you?

http://www.cdc.gov/DES/consumers/research/recent_hypospadias.html

But suppose in addition that I have hypospadias. And my mother possibly also had hypospadias. Do you begin to see zebra-stripes off in the distance?

When one hears hoofbeats one should look for horses not zebras. So when I saw your numbers the first issue is you did get ACTH, you did not get enough or what you got was out of date.

Should be easy to te st if this is possible. Give ACTH and see if your peripheral cortisol goes up. Called an ACTH Stimulation test.

I have a beer that it will be normal.

[Guest guest]

I see -- you think the hypospadias could be connected to the DES. Could the hyperaldo also be connected to DES? Is that what you're suggesting?

AG

[Guest guest]

Guess you did not read my evolution article?If that were the case the genome studies they have done in Pimas should have shown it.CE Grim MDI'm in Atlanta and I do not have diabetes. My a1c has always been acceptable. I only mention the diabetes because Roper's book is where I first saw the diagram of adrenal hormone pathways and recognized that if Roper is correct, the difference between diabetes and hyperaldosteronism could be as small this single enzyme. Marcia Ruth Roper's book is here: http://books.google.com/books?id=NHom29q7jLsC & printsec=frontcover & dq=marcia+ruth+roper & source=bl & ots=BulZDWAFom & sig=ZqO-FPCXVxYf1Pdl2USNEqEyBfs & hl=en & ei=8DUFTbGUJoSclgfVorywBw & sa=X & oi=book_result & ct=result & resnum=1 & ved=0CBMQ6AEwAA#v=onepage & q & f=false If the link doesn't work, it is titled "Type 2 Diabetes: The Adrenal Gland Disease" and there are many other sources for it. I linked this one because you may be able to read some of the book online at this link. I'm not sure. I cannot find a website for Roper herself. Apart from this claim about congenital 17-hydroxylase deficiency in the southwest Native American population and caffeine's inhibition of 17-hydroxylase in the Native American population, I do not think the book contains anything that would surprise you or most other competent endocrinologists. It is basic diabetes-for-the-patient stuff. But come to think of it, her ideas about genetic adaption to heat in the southwest Native Americans may be related to your ideas about adaptation to heat in the African-American population. I don't know enough to be sure. But maybe you two would have some interesting discussions... AG You need another ACTH test with urines as well is my guess by someone who is expert in this. You want to establish the DX before RX. I forget where you are I might know someone. It is so rare that I have never seen one. Would be good to have in your intro a brief sketch of who you are so I can better keep track. My opinion is that the diabetes problem is from eating too much and not exercising enough mostly. But will try to review what she is saying. Does she have a web site. Of course PA and its early stages will also be associated with DM II as aldo increases insulin resisitance and low K impairs insulin release. The first pt had DM II that was cured for years but eventually returned as did HTN. CE Grim MD Thanks for providing that link, a. Now that I've looked a little farther, I see that this enzyme is called 17-hydroxylase and a deficiency can indeed be hereditary and it is one of the rarer recognized forms of congenital adrenal hyperplasia. In classic form, it produces early and severe disruptio n of sexual development. (If I didn't have so much brain fog, I would remember these things from earlier investigation. I used to be brilliant that way, but no longer.) However, it apparently occurs in many degrees of severity. And that is apparently the enzyme also discussed by Marcia Ruth Roper in her book about which I posted some weeks back, "Type 2 Diabetes: The Adrenal Disease." Recall that she works with the Native American population and claims that a hereditary disruption in this enzyme is the root of their hereditary predisposition toward Type 2 diabetes and, according to Roper, the cause of their high sensitivity to caffeine as a disruptor of blood sugar metabolism. In her population, the bottleneck is between Pathway 2 and Pathway 3. (See my earlier post.) In my, hypothetically, the bottleneck would be between Pathway 1 and Pathway 2 . Otherwise, the mechanism of native American diabetes is the same as the mechanism of primary aldosteronism caused by 17-hydroxylase deficiency or inhibition. (Roper claims caffeine is an inhibitor.) So I guess the question becomes, could my low cortisol under ACTH stimulation equally well indicate some degree of 17-hydroxylase deficiency and a mild form of CAH? Or would that have been unmissably obvious from other symptoms or tests by now? And if so, would it respond to dexamethasone or some other treatment? AG A month or two back, I posted numbers from my AVS. Fortunately Dr Grim recognized they showed a failure. To satisfy my endo, I got third opinion from another expert, this one also a nationally recognized authority like Dr Grim. For the time being, my endo has fired me, but I anticipate that might change. He's a good man and a good doc in a confusing situation and probably experience pressures from above and around to join a wall of silence and denial. http://hyperaldo-too.blogspot.com/2010/12/report-from-my-avs.html etc...

[Guest guest]

Well I would have googled hypospadias for example because have not thought about it for a long time. I have a beer on vitiligo.CE Grim MDI don't know if she took hormones. She died in 2001 and I am checking with my dad to find out whether it was the hypspadias or the vitiligo that we had in common. I know he said something long ago about her having my condition, too. Now the question is "which condition" -- vitiligo or hypospadias. I didn't even know myself that I had any abnormality until some offhand remark a PCP made during a physical when I was about 45. It's first-degree or even sub-first-degree but a urologist confirmed it is definitely hypospadias. My PCP and endo both know very definitely about my hypospadias because I made a big deal about finding out whether or not I was going to have to have a urinary catheter for the AVS. But if there is some potential connection from the hypospadias to the hyperaldo, they have no clue about that. And in fairness, I wouldn't necessarily expect them to know something *that* esoteric, as long as they are open to finding out. So what is the different kind of horse you are pondering? AG Ah but given that info I begin to think of a different type of horse. A physical exam would have also added that info if done carefully. Don't know the genetics of hypospadias. Did not even know women could get it. Always learning something. Did she take hormones when pregnant with you? http://www.cdc.gov/DES/consumers/research/recent_hypospadias.html On Dec 12, 2010, at 1:21 PM, Alden wrote: But suppose in addition that I have hypospadias. And my mother possibly also had hypospadias. Do you begin to see zebra-stripes off in the distance? When one hears hoofbeats one should look for horses not zebras. So when I saw your numbers the first issue is you did get ACTH, you did not get enough or what you got was out of date. Should be easy to te st if this is possible. Give ACTH and see if your peripheral cortisol goes up. Called an ACTH Stimulation test. I have a beer that it will be normal.

[Guest guest]

Data links hypospad.Never thought about hyperaldo.Another good reason for a data base.So for each new question like this we raise we add the question such as do you have hypospadius? and send this to all members and they go to database and update. But would need thousands probably to see anything.Would be beautiful.I see -- you think the hypospadias could be connected to the DES. Could the hyperaldo also be connected to DES? Is that what you're suggesting? AG

[Guest guest]

Have read the evolution article more than once, it is only that I have a hard time making it stick. In addition to the pre-stroke aldo fog, I now have something much like Meniere's and the vertigo makes it hard to focus on my own concepts and sometimes damn near impossible to absorb other people's concepts. An email or letter is about the biggest complexity I am able to hold together most of the time.

There was no recognized damage to cognitive areas of the brain and when the symptoms subside I can sometimes have very clear days. But mostly not.

I believe Roper does say that genetic studies have shown what she's talking about but I can't hold such details in my head very well any more.

Guess you did not read my evolution article?

If that were the case the genome studies they have done in Pimas should have shown it.

CE Grim MD

I'm in Atlanta and I do not have diabetes. My a1c has always bee n acceptable.

I only mention the diabetes because Roper's book is where I first saw the diagram of adrenal hormone pathways and recognized that if Roper is correct, the difference between diabetes and hyperaldosteronism could be as small this single enzyme.

Marcia Ruth Roper's book is here:

http://books.google.com/books?id=NHom29q7jLsC & printsec=frontcover & dq=marcia+ruth+roper & source=bl & ots=BulZDWAFom & sig=ZqO-FPCXVxYf1Pdl2USNEqEyBfs & hl=en & ei=8DUFTbGUJoSclgfVorywBw & sa=X & oi=book_result & ct=result & resnum= 1 & ved=0CBMQ6AEwAA#v=onepage & q & f=false

[Guest guest]

The evolution article needs to be read with a pencil and paper in hand to sketch out the changes. I have an aninmated ppt that shows it as well and am working on getting it set up so folks can view it at Microsoft live site. Can't do this on Yahoo that I can tell. I can try sending it to your reg email as an attachment if you want but I need to do a voice over first I think.CE Grim MDHave read the evolution article more than once, it is only that I have a hard time making it stick. In addition to the pre-stroke aldo fog, I now have something much like Meniere's and the vertigo makes it hard to focus on my own concepts and sometimes damn near impossible to absorb other people's concepts. An email or letter is about the biggest complexity I am able to hold together most of the time. There was no recognized damage to cognitive areas of the brain and when the symptoms subside I can sometimes have very clear days. But mostly not. I believe Roper does say that genetic studies have shown what she's talking about but I can't hold such details in my head very well any more. Guess you did not read my evolution article? If that were the case the genome studies they have done in Pimas should have shown it. CE Grim MD I'm in Atlanta and I do not have diabetes. My a1c has always bee n acceptable. I only mention the diabetes because Roper's book is where I first saw the diagram of adrenal hormone pathways and recognized that if Roper is correct, the difference between diabetes and hyperaldosteronism could be as small this single enzyme. Marcia Ruth Roper's book is here: http://books.google.com/books?id=NHom29q7jLsC & printsec=frontcover & dq=marcia+ruth+roper & source=bl & ots=BulZDWAFom & sig=ZqO-FPCXVxYf1Pdl2USNEqEyBfs & hl=en & ei=8DUFTbGUJoSclgfVorywBw & sa=X & oi=book_result & ct=result & resnum= 1 & ved=0CBMQ6AEwAA#v=onepage & q & f=false

[Guest guest]

The evolution article needs to be read with a pencil and paper in hand to sketch out the changes. I have an aninmated ppt that shows it as well and am working on getting it set up so folks can view it at Microsoft live site. Can't do this on Yahoo that I can tell. I can try sending it to your reg email as an attachment if you want but I need to do a voice over first I think.CE Grim MDHave read the evolution article more than once, it is only that I have a hard time making it stick. In addition to the pre-stroke aldo fog, I now have something much like Meniere's and the vertigo makes it hard to focus on my own concepts and sometimes damn near impossible to absorb other people's concepts. An email or letter is about the biggest complexity I am able to hold together most of the time. There was no recognized damage to cognitive areas of the brain and when the symptoms subside I can sometimes have very clear days. But mostly not. I believe Roper does say that genetic studies have shown what she's talking about but I can't hold such details in my head very well any more. Guess you did not read my evolution article? If that were the case the genome studies they have done in Pimas should have shown it. CE Grim MD I'm in Atlanta and I do not have diabetes. My a1c has always bee n acceptable. I only mention the diabetes because Roper's book is where I first saw the diagram of adrenal hormone pathways and recognized that if Roper is correct, the difference between diabetes and hyperaldosteronism could be as small this single enzyme. Marcia Ruth Roper's book is here: http://books.google.com/books?id=NHom29q7jLsC & printsec=frontcover & dq=marcia+ruth+roper & source=bl & ots=BulZDWAFom & sig=ZqO-FPCXVxYf1Pdl2USNEqEyBfs & hl=en & ei=8DUFTbGUJoSclgfVorywBw & sa=X & oi=book_result & ct=result & resnum= 1 & ved=0CBMQ6AEwAA#v=onepage & q & f=false

[Guest guest]

My guess is that the largest number you can find in in our files here.We have 52 proven cases but not all have their results in there. All of our posts (30,000 or so) are searchable. Another reason we need a good data base. A month or two back, I posted numbers from my AVS. Fortunately Dr Grim recognized they showed a failure. To satisfy my endo, I got third opinion from another expert, this one also a nationally recognized authority like Dr Grim. For the time being, my endo has fired me, but I anticipate that might change. He's a good man and a good doc in a confusing situation and probably experience pressures from above and around to join a wall of silence and denial. http://hyperaldo-too.blogspot.com/2010/12/report-from-my-avs.html I have gone looking for other AVS reports on the web with little success, so I have two questions: 1) Is there a place where I can see two dozen or more AVS reports on the web? 2) From the few AVS reports I HAVE found, I gather that my cortisol numbers are 1/10 or 1/20 of the ballpark one would expect under ACTH stimulation. (Dr Grim noted earlier there must have been some problem with the ACTH stimulation.) I was also on 100 mg (half my usual dose) of eplerenone. But just suppose there was no glitch in administering the ACTH. Does this suggest an inhibition or deficiency in the enzyme P450-17alpha, the enzyme #3 that "passes along" hormones from "pathway 1" to "pathway 2" in the diagram here: http://www.dshs.state.tx.us/newborn/prenatal.shtm I link the article for the relevance of the diagram, not the relevance of the article, which seems (on superficial examination) to examine some other deficiency. The secondary sex characteristics are mildly attenuated in males in my family, and those characteristics come from pathway 3. If it is hard to reach pathway 2, then it is also hard to reach pathway 3.Do they have kids? If so prob OK If raw materials cannot get passed from pathway 1 to pathway 2, then the patient ends up with too much aldosterone, is that correct? Is P450-17alpha inhibition or deficiency one of the recognized familial problems? (Is it GRA?) Are other causes of it known? Even if not, is it recognized as a distinctive mechanism of hyperaldosteronism? Is there a specialized treatment for it? Thanks for any and all perspective,AG

[Guest guest]

all the time i get weak.i eat 3 times a day of meal.i don't drink much water.if i estimate it,i cannot consume 6 glass of water.The doctor haven't check my glucose.i loss weight. my weight now is 43kg.before i was in my 50 kg.what can u suggest? A month or two back, I posted numbers from my AVS. Fortunately Dr Grim recognized they showed a failure. To satisfy my endo, I got third opinion from another expert, this one also a nationally recognized authority like Dr Grim. For the time being, my endo has fired me, but I anticipate that might change. He's a good man and a good doc in a confusing situation and probably experience pressures from above and around to join a wall of silence and denial. http://hyperaldo-too.blogspot.com/2010/12/report-from-my-avs.html I have gone looking for other AVS reports on the web with little success, so I

have two questions: 1) Is there a place where I can see two dozen or more AVS reports on the web? 2) From the few AVS reports I HAVE found, I gather that my cortisol numbers are 1/10 or 1/20 of the ballpark one would expect under ACTH stimulation. (Dr Grim noted earlier there must have been some problem with the ACTH stimulation.) I was also on 100 mg (half my usual dose) of eplerenone. But just suppose there was no glitch in administering the ACTH. Does this suggest an inhibition or deficiency in the enzyme P450-17alpha, the enzyme #3 that "passes along" hormones from "pathway 1" to "pathway 2" in the diagram here: http://www.dshs.state.tx.us/newborn/prenatal.shtm I link the

article for the relevance of the diagram, not the relevance of the article, which seems (on superficial examination) to examine some other deficiency. The secondary sex characteristics are mildly attenuated in males in my family, and those characteristics come from pathway 3. If it is hard to reach pathway 2, then it is also hard to reach pathway 3.Do they have kids? If so prob OK If raw materials cannot get passed from pathway 1 to pathway 2, then the patient ends up with too much aldosterone, is that correct? Is P450-17alpha inhibition or deficiency one of the recognized familial problems? (Is it GRA?) Are other causes of it known? Even if not, is it recognized as a distinctive mechanism of hyperaldosteronism? Is there a specialized treatment for it? Thanks for any and all perspective,AG