Re: Failed AVS Redux

[Guest guest]

DASH like your life depended on itGet the book. Amazon.com has it.CE Grim MDall 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

[Guest guest]

ok i will,it is just that i took a glimpse and saw the menu on DASH net. It is like that some of it are hard to find here at Baguio.Well, i am still reviewing for my board exam this coming Jan. that's why i haven't see my doctor yet.Thanks. 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]

You can also do the rice fruit diet there. See Ricediet.comTiped sad Send form miiPhone ;-)May your pressure be low!CE Grim MDSpecializing in DifficultHypertension

ok i will,it is just that i took a glimpse and saw the menu on DASH net. It is like that some of it are hard to find here at Baguio.Well, i am still reviewing for my board exam this coming Jan. that's why i haven't see my doctor yet.Thanks. 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