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Posted by farshad on March 18, 2018, at 16:23:09
In reply to Re: How can I block Cortisol? » farshad, posted by ed_uk2010 on March 18, 2018, at 16:17:35
> So why aren't you seeing a specialist/psychiatrist?
they refuse to help me and say I should just go the therapy route since no meds work for me.
Posted by ed_uk2010 on March 18, 2018, at 16:33:27
In reply to Re: How can I block Cortisol?, posted by farshad on March 18, 2018, at 16:23:09
> > So why aren't you seeing a specialist/psychiatrist?
So, meds like pramipexole, did you buy online?
Posted by farshad on March 18, 2018, at 16:41:55
In reply to Re: How can I block Cortisol?, posted by ed_uk2010 on March 18, 2018, at 16:33:27
> > > So why aren't you seeing a specialist/psychiatrist?
>
> So, meds like pramipexole, did you buy online?
>yeah I get them all online besides wellbutrin which I get from my doctor .
Posted by ed_uk2010 on March 18, 2018, at 16:46:34
In reply to Re: How can I block Cortisol?, posted by farshad on March 18, 2018, at 16:41:55
So have you been referred to someone for the endocrine tests?
Posted by farshad on March 18, 2018, at 16:47:48
In reply to Re: How can I block Cortisol? » farshad, posted by ed_uk2010 on March 18, 2018, at 16:46:34
> So have you been referred to someone for the endocrine tests?
>family doctor which I get my wellbutrin from
Posted by SLS on March 19, 2018, at 8:43:45
In reply to Re: How can I block Cortisol?, posted by ed_uk2010 on March 18, 2018, at 16:33:27
For what it's worth, I tried mifepristone for 8 consecutive days. It did not help with depression at all. However, by the eighth day, I felt washed-out and unwell. The protocol at the time called for treatment of a short duration so as not to not cause adrenal exhaustion. Although I do not have psychotic depression, I thought that it was worth a try.
- Scott
Posted by farshad on March 19, 2018, at 14:13:05
In reply to Re: How can I block Cortisol?, posted by SLS on March 19, 2018, at 8:43:45
has anyone seen this study ? its from 1998 . I think they are suggesting there could be CRF1 mutations but unrelated to cushings disease>
I quote from the study ...No mutations affecting the CRF1-R protein have been found in all tumors analyzed. However, we found a significant overexpression of the CRF1-R messenger RNA in ACTH-secreting pituitary adenomas vs. inactive adenomas and normal pituitaries. We conclude that mutations of the CRF1-R are unlikely to be involved in Cushing's disease. We suggest that the overexpression of the CRF1-R messenger RNA may be related to a disturbed receptor regulation in ACTH-secreting pituitary adenomas...
https://www.ncbi.nlm.nih.gov/pubmed/9745449
English is my 3rd language so maybe someone can explain this that understands it better_
Posted by farshad on March 19, 2018, at 14:16:15
In reply to Re: How can I block Cortisol?, posted by farshad on March 19, 2018, at 14:13:05
> has anyone seen this study ? its from 1998 . I think they are suggesting there could be CRF1 mutations but unrelated to cushings disease>
>
> I quote from the study ...No mutations affecting the CRF1-R protein have been found in all tumors analyzed. However, we found a significant overexpression of the CRF1-R messenger RNA in ACTH-secreting pituitary adenomas vs. inactive adenomas and normal pituitaries. We conclude that mutations of the CRF1-R are unlikely to be involved in Cushing's disease. We suggest that the overexpression of the CRF1-R messenger RNA may be related to a disturbed receptor regulation in ACTH-secreting pituitary adenomas...
>
> https://www.ncbi.nlm.nih.gov/pubmed/9745449
>
> English is my 3rd language so maybe someone can explain this that understands it better_I found 2 possible mutations that I have related to ACTH>
PDE8B https://www.selfdecode.com/gene/pde8b/#advanced-summary
ACE (Angiotensin I converting enzyme) https://www.selfdecode.com/gene/ace/
Posted by farshad on March 19, 2018, at 14:20:38
In reply to Re: How can I block Cortisol?, posted by farshad on March 19, 2018, at 14:16:15
> > has anyone seen this study ? its from 1998 . I think they are suggesting there could be CRF1 mutations but unrelated to cushings disease>
> >
> > I quote from the study ...No mutations affecting the CRF1-R protein have been found in all tumors analyzed. However, we found a significant overexpression of the CRF1-R messenger RNA in ACTH-secreting pituitary adenomas vs. inactive adenomas and normal pituitaries. We conclude that mutations of the CRF1-R are unlikely to be involved in Cushing's disease. We suggest that the overexpression of the CRF1-R messenger RNA may be related to a disturbed receptor regulation in ACTH-secreting pituitary adenomas...
> >
> > https://www.ncbi.nlm.nih.gov/pubmed/9745449
> >
> > English is my 3rd language so maybe someone can explain this that understands it better_
>
> I found 2 possible mutations that I have related to ACTH>
>
> PDE8B https://www.selfdecode.com/gene/pde8b/#advanced-summary
>
> ACE (Angiotensin I converting enzyme) https://www.selfdecode.com/gene/ace/--------------
One mutation in human PDE8B (His350Pro), from a patient with severe adrenal hyperplasia, impaired PDE8B catalytic activity, and its expression in Hela cells resulted in increased cAMP-signaling, suggesting a role for cAMP in development of adrenal hyprerplasia. Such PDE8B mutations may not directly cause adrenal hyperplasia, however, since PDE8B KO mice do not develop adrenal tumors (Tsai and Beavo 2011). Inactivating PDE11A gene mutations are also associated with the development of adrenal hyperplasia and Cushing syndrome (Libe et al. 2008), and with Carney complex (CNC). CNC is caused by germline mutations in the alpha regulatory subunit of PKA (PRKARIA) and is associated with endocrine tumors, including nodular adrenal hyperplasia and adrenal and testicular tumors (Levy et al. 2011;Libe et al. 2011). PDE11A mutations may also play a role in susceptibility to prostate cancer (Faucz et al. 2011) and testicular germ cell tumors (TGCT) (Horvath et al. 2009).
------------https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4275405/
https://en.wikipedia.org/wiki/Congenital_adrenal_hyperplasia
Posted by farshad on March 19, 2018, at 14:29:45
In reply to Re: How can I block Cortisol?, posted by farshad on March 19, 2018, at 14:20:38
> > > has anyone seen this study ? its from 1998 . I think they are suggesting there could be CRF1 mutations but unrelated to cushings disease>
> > >
> > > I quote from the study ...No mutations affecting the CRF1-R protein have been found in all tumors analyzed. However, we found a significant overexpression of the CRF1-R messenger RNA in ACTH-secreting pituitary adenomas vs. inactive adenomas and normal pituitaries. We conclude that mutations of the CRF1-R are unlikely to be involved in Cushing's disease. We suggest that the overexpression of the CRF1-R messenger RNA may be related to a disturbed receptor regulation in ACTH-secreting pituitary adenomas...
> > >
> > > https://www.ncbi.nlm.nih.gov/pubmed/9745449
> > >
> > > English is my 3rd language so maybe someone can explain this that understands it better_
> >
> > I found 2 possible mutations that I have related to ACTH>
> >
> > PDE8B https://www.selfdecode.com/gene/pde8b/#advanced-summary
> >
> > ACE (Angiotensin I converting enzyme) https://www.selfdecode.com/gene/ace/
>
> --------------
> One mutation in human PDE8B (His350Pro), from a patient with severe adrenal hyperplasia, impaired PDE8B catalytic activity, and its expression in Hela cells resulted in increased cAMP-signaling, suggesting a role for cAMP in development of adrenal hyprerplasia. Such PDE8B mutations may not directly cause adrenal hyperplasia, however, since PDE8B KO mice do not develop adrenal tumors (Tsai and Beavo 2011). Inactivating PDE11A gene mutations are also associated with the development of adrenal hyperplasia and Cushing syndrome (Libe et al. 2008), and with Carney complex (CNC). CNC is caused by germline mutations in the alpha regulatory subunit of PKA (PRKARIA) and is associated with endocrine tumors, including nodular adrenal hyperplasia and adrenal and testicular tumors (Levy et al. 2011;Libe et al. 2011). PDE11A mutations may also play a role in susceptibility to prostate cancer (Faucz et al. 2011) and testicular germ cell tumors (TGCT) (Horvath et al. 2009).
> ------------
>
> https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4275405/
>
>
> https://en.wikipedia.org/wiki/Congenital_adrenal_hyperplasia
>https://en.wikipedia.org/wiki/Angiotensin (Angiotensin I converting enzyme)
Posted by farshad on March 19, 2018, at 14:35:21
In reply to Re: How can I block Cortisol? » farshad, posted by farshad on March 19, 2018, at 14:29:45
> > > > has anyone seen this study ? its from 1998 . I think they are suggesting there could be CRF1 mutations but unrelated to cushings disease>
> > > >
> > > > I quote from the study ...No mutations affecting the CRF1-R protein have been found in all tumors analyzed. However, we found a significant overexpression of the CRF1-R messenger RNA in ACTH-secreting pituitary adenomas vs. inactive adenomas and normal pituitaries. We conclude that mutations of the CRF1-R are unlikely to be involved in Cushing's disease. We suggest that the overexpression of the CRF1-R messenger RNA may be related to a disturbed receptor regulation in ACTH-secreting pituitary adenomas...
> > > >
> > > > https://www.ncbi.nlm.nih.gov/pubmed/9745449
> > > >
> > > > English is my 3rd language so maybe someone can explain this that understands it better_
> > >
> > > I found 2 possible mutations that I have related to ACTH>
> > >
> > > PDE8B https://www.selfdecode.com/gene/pde8b/#advanced-summary
> > >
> > > ACE (Angiotensin I converting enzyme) https://www.selfdecode.com/gene/ace/
> >
> > --------------
> > One mutation in human PDE8B (His350Pro), from a patient with severe adrenal hyperplasia, impaired PDE8B catalytic activity, and its expression in Hela cells resulted in increased cAMP-signaling, suggesting a role for cAMP in development of adrenal hyprerplasia. Such PDE8B mutations may not directly cause adrenal hyperplasia, however, since PDE8B KO mice do not develop adrenal tumors (Tsai and Beavo 2011). Inactivating PDE11A gene mutations are also associated with the development of adrenal hyperplasia and Cushing syndrome (Libe et al. 2008), and with Carney complex (CNC). CNC is caused by germline mutations in the alpha regulatory subunit of PKA (PRKARIA) and is associated with endocrine tumors, including nodular adrenal hyperplasia and adrenal and testicular tumors (Levy et al. 2011;Libe et al. 2011). PDE11A mutations may also play a role in susceptibility to prostate cancer (Faucz et al. 2011) and testicular germ cell tumors (TGCT) (Horvath et al. 2009).
> > ------------
> >
> > https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4275405/
> >
> >
> > https://en.wikipedia.org/wiki/Congenital_adrenal_hyperplasia
> >
>
> https://en.wikipedia.org/wiki/Angiotensin (Angiotensin I converting enzyme)
I dont know what to think this is all so confusing. So I have mutations in my CRF1 gene specifically with the PDE8B causing excessive cortisol and the Secretion of CRH, ACTH, and cortisol is increased by stimulation of angiotensin AT(1) receptors.So it all goes in a loop and just further pushes each other to the max?
Posted by farshad on March 19, 2018, at 14:40:31
In reply to Re: How can I block Cortisol?, posted by farshad on March 19, 2018, at 14:35:21
> > > > > has anyone seen this study ? its from 1998 . I think they are suggesting there could be CRF1 mutations but unrelated to cushings disease>
> > > > >
> > > > > I quote from the study ...No mutations affecting the CRF1-R protein have been found in all tumors analyzed. However, we found a significant overexpression of the CRF1-R messenger RNA in ACTH-secreting pituitary adenomas vs. inactive adenomas and normal pituitaries. We conclude that mutations of the CRF1-R are unlikely to be involved in Cushing's disease. We suggest that the overexpression of the CRF1-R messenger RNA may be related to a disturbed receptor regulation in ACTH-secreting pituitary adenomas...
> > > > >
> > > > > https://www.ncbi.nlm.nih.gov/pubmed/9745449
> > > > >
> > > > > English is my 3rd language so maybe someone can explain this that understands it better_
> > > >
> > > > I found 2 possible mutations that I have related to ACTH>
> > > >
> > > > PDE8B https://www.selfdecode.com/gene/pde8b/#advanced-summary
> > > >
> > > > ACE (Angiotensin I converting enzyme) https://www.selfdecode.com/gene/ace/
> > >
> > > --------------
> > > One mutation in human PDE8B (His350Pro), from a patient with severe adrenal hyperplasia, impaired PDE8B catalytic activity, and its expression in Hela cells resulted in increased cAMP-signaling, suggesting a role for cAMP in development of adrenal hyprerplasia. Such PDE8B mutations may not directly cause adrenal hyperplasia, however, since PDE8B KO mice do not develop adrenal tumors (Tsai and Beavo 2011). Inactivating PDE11A gene mutations are also associated with the development of adrenal hyperplasia and Cushing syndrome (Libe et al. 2008), and with Carney complex (CNC). CNC is caused by germline mutations in the alpha regulatory subunit of PKA (PRKARIA) and is associated with endocrine tumors, including nodular adrenal hyperplasia and adrenal and testicular tumors (Levy et al. 2011;Libe et al. 2011). PDE11A mutations may also play a role in susceptibility to prostate cancer (Faucz et al. 2011) and testicular germ cell tumors (TGCT) (Horvath et al. 2009).
> > > ------------
> > >
> > > https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4275405/
> > >
> > >
> > > https://en.wikipedia.org/wiki/Congenital_adrenal_hyperplasia
> > >
> >
> > https://en.wikipedia.org/wiki/Angiotensin (Angiotensin I converting enzyme)
>
>
> I dont know what to think this is all so confusing. So I have mutations in my CRF1 gene specifically with the PDE8B causing excessive cortisol and the Secretion of CRH, ACTH, and cortisol is increased by stimulation of angiotensin AT(1) receptors.
>
> So it all goes in a loop and just further pushes each other to the max?
>
here are the 2 CRF1 mutations btw
https://www.selfdecode.com/gene/crhr1-it1/
https://www.selfdecode.com/gene/mgc57346-crhr1/
Posted by farshad on March 19, 2018, at 15:16:20
In reply to Re: How can I block Cortisol?, posted by farshad on March 19, 2018, at 14:40:31
> > > > > > has anyone seen this study ? its from 1998 . I think they are suggesting there could be CRF1 mutations but unrelated to cushings disease>
> > > > > >
> > > > > > I quote from the study ...No mutations affecting the CRF1-R protein have been found in all tumors analyzed. However, we found a significant overexpression of the CRF1-R messenger RNA in ACTH-secreting pituitary adenomas vs. inactive adenomas and normal pituitaries. We conclude that mutations of the CRF1-R are unlikely to be involved in Cushing's disease. We suggest that the overexpression of the CRF1-R messenger RNA may be related to a disturbed receptor regulation in ACTH-secreting pituitary adenomas...
> > > > > >
> > > > > > https://www.ncbi.nlm.nih.gov/pubmed/9745449
> > > > > >
> > > > > > English is my 3rd language so maybe someone can explain this that understands it better_
> > > > >
> > > > > I found 2 possible mutations that I have related to ACTH>
> > > > >
> > > > > PDE8B https://www.selfdecode.com/gene/pde8b/#advanced-summary
> > > > >
> > > > > ACE (Angiotensin I converting enzyme) https://www.selfdecode.com/gene/ace/
> > > >
> > > > --------------
> > > > One mutation in human PDE8B (His350Pro), from a patient with severe adrenal hyperplasia, impaired PDE8B catalytic activity, and its expression in Hela cells resulted in increased cAMP-signaling, suggesting a role for cAMP in development of adrenal hyprerplasia. Such PDE8B mutations may not directly cause adrenal hyperplasia, however, since PDE8B KO mice do not develop adrenal tumors (Tsai and Beavo 2011). Inactivating PDE11A gene mutations are also associated with the development of adrenal hyperplasia and Cushing syndrome (Libe et al. 2008), and with Carney complex (CNC). CNC is caused by germline mutations in the alpha regulatory subunit of PKA (PRKARIA) and is associated with endocrine tumors, including nodular adrenal hyperplasia and adrenal and testicular tumors (Levy et al. 2011;Libe et al. 2011). PDE11A mutations may also play a role in susceptibility to prostate cancer (Faucz et al. 2011) and testicular germ cell tumors (TGCT) (Horvath et al. 2009).
> > > > ------------
> > > >
> > > > https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4275405/
> > > >
> > > >
> > > > https://en.wikipedia.org/wiki/Congenital_adrenal_hyperplasia
> > > >
> > >
> > > https://en.wikipedia.org/wiki/Angiotensin (Angiotensin I converting enzyme)
> >
> >
> > I dont know what to think this is all so confusing. So I have mutations in my CRF1 gene specifically with the PDE8B causing excessive cortisol and the Secretion of CRH, ACTH, and cortisol is increased by stimulation of angiotensin AT(1) receptors.
> >
> > So it all goes in a loop and just further pushes each other to the max?
> >
> here are the 2 CRF1 mutations btw
> https://www.selfdecode.com/gene/crhr1-it1/
> https://www.selfdecode.com/gene/mgc57346-crhr1/
>
So its obvious that there is something wrong with my genetics specificaly the cortisol/fight or flight stress related ones, which is why I think I have such bad anxiety . Can anyone help me out so I can understand this simple?
Here are some other cortisol genes I found I have problems with(does this make sense to anyone?):
https://www.selfdecode.com/gene/gnas/#advanced-summary - Constitutive activation of the adenylate cyclase enzyme leads to over-production of several hormones IE cortisol?
https://www.selfdecode.com/gene/nr3c2/#advanced-summary - Mutations in the NR3C2 gene lead to a nonfunctional or abnormally functioning mineralocorticoid receptor protein that cannot properly regulate the specialized proteins that transport sodium and potassium
2 others
https://www.selfdecode.com/gene/h6pd/#advanced-summary%C2%A0%C2%A0
Posted by farshad on March 19, 2018, at 15:30:37
In reply to Re: How can I block Cortisol?, posted by farshad on March 19, 2018, at 15:16:20
> > > > > > > has anyone seen this study ? its from 1998 . I think they are suggesting there could be CRF1 mutations but unrelated to cushings disease>
> > > > > > >
> > > > > > > I quote from the study ...No mutations affecting the CRF1-R protein have been found in all tumors analyzed. However, we found a significant overexpression of the CRF1-R messenger RNA in ACTH-secreting pituitary adenomas vs. inactive adenomas and normal pituitaries. We conclude that mutations of the CRF1-R are unlikely to be involved in Cushing's disease. We suggest that the overexpression of the CRF1-R messenger RNA may be related to a disturbed receptor regulation in ACTH-secreting pituitary adenomas...
> > > > > > >
> > > > > > > https://www.ncbi.nlm.nih.gov/pubmed/9745449
> > > > > > >
> > > > > > > English is my 3rd language so maybe someone can explain this that understands it better_
> > > > > >
> > > > > > I found 2 possible mutations that I have related to ACTH>
> > > > > >
> > > > > > PDE8B https://www.selfdecode.com/gene/pde8b/#advanced-summary
> > > > > >
> > > > > > ACE (Angiotensin I converting enzyme) https://www.selfdecode.com/gene/ace/
> > > > >
> > > > > --------------
> > > > > One mutation in human PDE8B (His350Pro), from a patient with severe adrenal hyperplasia, impaired PDE8B catalytic activity, and its expression in Hela cells resulted in increased cAMP-signaling, suggesting a role for cAMP in development of adrenal hyprerplasia. Such PDE8B mutations may not directly cause adrenal hyperplasia, however, since PDE8B KO mice do not develop adrenal tumors (Tsai and Beavo 2011). Inactivating PDE11A gene mutations are also associated with the development of adrenal hyperplasia and Cushing syndrome (Libe et al. 2008), and with Carney complex (CNC). CNC is caused by germline mutations in the alpha regulatory subunit of PKA (PRKARIA) and is associated with endocrine tumors, including nodular adrenal hyperplasia and adrenal and testicular tumors (Levy et al. 2011;Libe et al. 2011). PDE11A mutations may also play a role in susceptibility to prostate cancer (Faucz et al. 2011) and testicular germ cell tumors (TGCT) (Horvath et al. 2009).
> > > > > ------------
> > > > >
> > > > > https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4275405/
> > > > >
> > > > >
> > > > > https://en.wikipedia.org/wiki/Congenital_adrenal_hyperplasia
> > > > >
> > > >
> > > > https://en.wikipedia.org/wiki/Angiotensin (Angiotensin I converting enzyme)
> > >
> > >
> > > I dont know what to think this is all so confusing. So I have mutations in my CRF1 gene specifically with the PDE8B causing excessive cortisol and the Secretion of CRH, ACTH, and cortisol is increased by stimulation of angiotensin AT(1) receptors.
> > >
> > > So it all goes in a loop and just further pushes each other to the max?
> > >
> > here are the 2 CRF1 mutations btw
> > https://www.selfdecode.com/gene/crhr1-it1/
> > https://www.selfdecode.com/gene/mgc57346-crhr1/
> >
>
>
> So its obvious that there is something wrong with my genetics specificaly the cortisol/fight or flight stress related ones, which is why I think I have such bad anxiety . Can anyone help me out so I can understand this simple?
>
> Here are some other cortisol genes I found I have problems with(does this make sense to anyone?):
>
>
>
> https://www.selfdecode.com/gene/gnas/#advanced-summary - Constitutive activation of the adenylate cyclase enzyme leads to over-production of several hormones IE cortisol?
>
>
>
> https://www.selfdecode.com/gene/nr3c2/#advanced-summary - Mutations in the NR3C2 gene lead to a nonfunctional or abnormally functioning mineralocorticoid receptor protein that cannot properly regulate the specialized proteins that transport sodium and potassium
>
>
>
>
>
> 2 others
>
>
>
> https://www.selfdecode.com/gene/h6pd/#advanced-summary%C2%A0%C2%A0
>
>
>
> https://www.selfdecode.com/gene/serpina6/#advanced-summaryDo you guys think all of this can be fixed just by taking Metyrapone? Since it blocks cortisol.
Posted by farshad on March 19, 2018, at 16:30:38
In reply to Re: How can I block Cortisol?, posted by farshad on March 19, 2018, at 15:30:37
> > > > > > > > has anyone seen this study ? its from 1998 . I think they are suggesting there could be CRF1 mutations but unrelated to cushings disease>
> > > > > > > >
> > > > > > > > I quote from the study ...No mutations affecting the CRF1-R protein have been found in all tumors analyzed. However, we found a significant overexpression of the CRF1-R messenger RNA in ACTH-secreting pituitary adenomas vs. inactive adenomas and normal pituitaries. We conclude that mutations of the CRF1-R are unlikely to be involved in Cushing's disease. We suggest that the overexpression of the CRF1-R messenger RNA may be related to a disturbed receptor regulation in ACTH-secreting pituitary adenomas...
> > > > > > > >
> > > > > > > > https://www.ncbi.nlm.nih.gov/pubmed/9745449
> > > > > > > >
> > > > > > > > English is my 3rd language so maybe someone can explain this that understands it better_
> > > > > > >
> > > > > > > I found 2 possible mutations that I have related to ACTH>
> > > > > > >
> > > > > > > PDE8B https://www.selfdecode.com/gene/pde8b/#advanced-summary
> > > > > > >
> > > > > > > ACE (Angiotensin I converting enzyme) https://www.selfdecode.com/gene/ace/
> > > > > >
> > > > > > --------------
> > > > > > One mutation in human PDE8B (His350Pro), from a patient with severe adrenal hyperplasia, impaired PDE8B catalytic activity, and its expression in Hela cells resulted in increased cAMP-signaling, suggesting a role for cAMP in development of adrenal hyprerplasia. Such PDE8B mutations may not directly cause adrenal hyperplasia, however, since PDE8B KO mice do not develop adrenal tumors (Tsai and Beavo 2011). Inactivating PDE11A gene mutations are also associated with the development of adrenal hyperplasia and Cushing syndrome (Libe et al. 2008), and with Carney complex (CNC). CNC is caused by germline mutations in the alpha regulatory subunit of PKA (PRKARIA) and is associated with endocrine tumors, including nodular adrenal hyperplasia and adrenal and testicular tumors (Levy et al. 2011;Libe et al. 2011). PDE11A mutations may also play a role in susceptibility to prostate cancer (Faucz et al. 2011) and testicular germ cell tumors (TGCT) (Horvath et al. 2009).
> > > > > > ------------
> > > > > >
> > > > > > https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4275405/
> > > > > >
> > > > > >
> > > > > > https://en.wikipedia.org/wiki/Congenital_adrenal_hyperplasia
> > > > > >
> > > > >
> > > > > https://en.wikipedia.org/wiki/Angiotensin (Angiotensin I converting enzyme)
> > > >
> > > >
> > > > I dont know what to think this is all so confusing. So I have mutations in my CRF1 gene specifically with the PDE8B causing excessive cortisol and the Secretion of CRH, ACTH, and cortisol is increased by stimulation of angiotensin AT(1) receptors.
> > > >
> > > > So it all goes in a loop and just further pushes each other to the max?
> > > >
> > > here are the 2 CRF1 mutations btw
> > > https://www.selfdecode.com/gene/crhr1-it1/
> > > https://www.selfdecode.com/gene/mgc57346-crhr1/
> > >
> >
> >
> > So its obvious that there is something wrong with my genetics specificaly the cortisol/fight or flight stress related ones, which is why I think I have such bad anxiety . Can anyone help me out so I can understand this simple?
> >
> > Here are some other cortisol genes I found I have problems with(does this make sense to anyone?):
> >
> >
> >
> > https://www.selfdecode.com/gene/gnas/#advanced-summary - Constitutive activation of the adenylate cyclase enzyme leads to over-production of several hormones IE cortisol?
> >
> >
> >
> > https://www.selfdecode.com/gene/nr3c2/#advanced-summary - Mutations in the NR3C2 gene lead to a nonfunctional or abnormally functioning mineralocorticoid receptor protein that cannot properly regulate the specialized proteins that transport sodium and potassium
> >
> >
> >
> >
> >
> > 2 others
> >
> >
> >
> > https://www.selfdecode.com/gene/h6pd/#advanced-summary%C2%A0%C2%A0
> >
> >
> >
> > https://www.selfdecode.com/gene/serpina6/#advanced-summary
>
> Do you guys think all of this can be fixed just by taking Metyrapone? Since it blocks cortisol.
How am I supposed to decipher all this?..
https://www.selfdeco...m/gene/cyp17a1/ - this condition affects the function of certain hormone-producing glands
https://www.selfdeco.../gene/ppargc1b/ - Activates transcritional activity of estrogen receptor alpha, nuclear respiratory factor 1 (NRF1) and glucocorticoid receptor in the presence of glucocorticoids.
https://www.selfdeco...m/gene/txnrd2/
https://www.selfdeco...dvanced-summary - adrenocorticotropic
Posted by Phillipa on March 19, 2018, at 18:08:43
In reply to Re: How can I block Cortisol?, posted by farshad on March 19, 2018, at 16:30:38
Hi what languages do you speak? I am no med expert. I looked at you first post link and googled this. Don't know if will help or not Phillipa
https://rarediseases.info.nih.gov/diseases/12867/acth-secreting-pituitary-adenoma
Posted by Lamdage22 on March 20, 2018, at 12:36:33
In reply to Re: How can I block Cortisol? » farshad, posted by Phillipa on March 19, 2018, at 18:08:43
how is cortisol measured? I may do the same test
Posted by ed_uk2010 on March 20, 2018, at 18:42:57
In reply to Re: How can I block Cortisol?, posted by Lamdage22 on March 20, 2018, at 12:36:33
> how is cortisol measured? I may do the same test
Cortisol levels vary greatly throughout the day and according to circumstances. You can't just measure the level randomly and get a useful result.
If cortisol is markedly elevated for a prolonged period, there are usually physical/medical symptoms as well as psychiatric symptoms. It would not be usual for a medical cause of high cortisol to present with psychiatric symptoms in isolation.
You would need to perform at least two of the below tests to identify an issue with elevated cortisol:
1. A 24 hour urine collection and analysis for cortisol content (this test is often done twice),
2. A late night saliva test for cortisol concentration,
3. An overnight dexamethasone suppression test with morning analysis of blood cortisol level.
You cannot perform a dexamethasone suppression test (no. 3) alone to look for a primary issue with cortisol. The normal suppressor pattern is often disrupted in severe depression (with or with anxiety) and in psychotic depression, with pts becoming non suppressors.
Posted by farshad on March 22, 2018, at 11:28:39
In reply to Re: How can I block Cortisol? » farshad, posted by ed_uk2010 on March 16, 2018, at 17:54:35
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> If tests demonstrated that you had an abnormally high level of cortisol, the first step would be to investigate the cause. Scans may be done to look for tumors on the adrenal glands (CT abdomen), or the pituitary (MRI head). Cortisol excess caused by tumors are sometimes treated with surgery. Medication is generally used when the condition is inoperable.
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>if I operate and remove the tumour Wont it just grow back ?
Also what else do you think could be causing high cortisol/acth besides a tumour and regular mental problems?
Posted by farshad on March 22, 2018, at 11:30:54
In reply to Re: How can I block Cortisol?, posted by farshad on March 22, 2018, at 11:28:39
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> > If tests demonstrated that you had an abnormally high level of cortisol, the first step would be to investigate the cause. Scans may be done to look for tumors on the adrenal glands (CT abdomen), or the pituitary (MRI head). Cortisol excess caused by tumors are sometimes treated with surgery. Medication is generally used when the condition is inoperable.
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> if I operate and remove the tumour Wont it just grow back ?also wouldnt i feel the tumour or how does that work? can you have a tumour anywhere? what causes tumours? what types of tumours are there or how many?
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> Also what else do you think could be causing high cortisol/acth besides a tumour and regular mental problems?
Posted by farshad on March 22, 2018, at 11:31:17
In reply to Re: How can I block Cortisol?, posted by farshad on March 22, 2018, at 11:30:54
> >
> > >
> > > If tests demonstrated that you had an abnormally high level of cortisol, the first step would be to investigate the cause. Scans may be done to look for tumors on the adrenal glands (CT abdomen), or the pituitary (MRI head). Cortisol excess caused by tumors are sometimes treated with surgery. Medication is generally used when the condition is inoperable.
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> > if I operate and remove the tumour Wont it just grow back ?also wouldnt i feel the tumour if I had 1 or how does that work? can you have a tumour anywhere? what causes tumours? what types of tumours are there or how many?
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> > Also what else do you think could be causing high cortisol/acth besides a tumour and regular mental problems?
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Posted by ed_uk2010 on March 22, 2018, at 16:39:33
In reply to Re: How can I block Cortisol?, posted by farshad on March 22, 2018, at 11:28:39
I seriously doubt you have a tumour.
You're obviously concerned about cortisol though. You'd have to have the tests to put your mind at rest.
Posted by baseball55 on March 22, 2018, at 18:16:47
In reply to Re: How can I block Cortisol?, posted by ed_uk2010 on March 22, 2018, at 16:39:33
You know, you seem to believe that your anxiety is caused by high cortisol. But the reality is that anxiety itself CAUSES high cortisol. People with Cushing's do not feel anxiety due to the high cortisol. You should look up the symptoms for Cushing's before you conclude that you have a cortisol problem.
Posted by Phillipa on March 22, 2018, at 20:06:25
In reply to Re: How can I block Cortisol?, posted by baseball55 on March 22, 2018, at 18:16:47
Posted by farshad on March 23, 2018, at 7:35:23
In reply to Re: How can I block Cortisol?, posted by baseball55 on March 22, 2018, at 18:16:47
> You know, you seem to believe that your anxiety is caused by high cortisol. But the reality is that anxiety itself CAUSES high cortisol. People with Cushing's do not feel anxiety due to the high cortisol. You should look up the symptoms for Cushing's before you conclude that you have a cortisol problem.
What people with chusings do not feel anxiety? how do u know?
also I said I have mutations in my cortisol/acth genes causing this high cortisol if not the tumour. or some autoimmune disorder. so eventually my cortisol would get high becuase of the mutations no matter what becuase you cant avoid stress.
https://www.ncbi.nlm.nih.gov/m/pubmed/20011602/https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3312460/
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1884405/
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