Re: depression and adverse cardiovascular events

[Guest guest]

From pubmed

Subchronic treatment with aldosterone induces depression-like behaviours and

gene expression changes relevant to major depressive disorder.

Hlavacova N, Wes PD, Ondrejcakova M, Flynn ME, Poundstone PK, Babic S, Murck H,

Jezova D.

SourceLaboratory of Pharmacological Neuroendocrinology, Institute of

Experimental Endocrinology, Slovak Academy of Sciences, Vlarska, Bratislava,

Slovakia.

Abstract

The potential role of aldosterone in the pathophysiology of depression is

unclear. The aim of this study was to test the hypothesis that prolonged

elevation of circulating aldosterone induces depression-like behaviour

accompanied by disease-relevant changes in gene expression in the hippocampus.

Subchronic (2-wk) treatment with aldosterone (2 & #956;g/100 g body weight per

day) or vehicle via subcutaneous osmotic minipumps was used to induce

hyperaldosteronism in male rats. All rats (n=20/treatment group) underwent a

modified sucrose preference test. Half of the animals from each treatment group

were exposed to the forced swim test (FST), which served both as a tool to

assess depression-like behaviour and as a stress stimulus. Affymetrix microarray

analysis was used to screen the entire rat genome for gene expression changes in

the hippocampus. Aldosterone treatment induced an anhedonic state manifested by

decreased sucrose preference. In the FST, depressogenic action of aldosterone

was manifested by decreased latency to immobility and increased time spent

immobile. Aldosterone treatment resulted in transcriptional changes of genes in

the hippocampus involved in inflammation, glutamatergic activity, and synaptic

and neuritic remodelling. Furthermore, aldosterone-regulated genes substantially

overlapped with genes affected by stress in the FST. This study demonstrates the

existence of a causal relationship between the hyperaldosteronism and depressive

behaviour. In addition, aldosterone treatment induced changes in gene expression

that may be relevant to the aetiology of major depressive disorder. Subchronic

treatment with aldosterone represents a new animal model of depression, which

may contribute to the development of novel targets for the treatment of

depression.

>

> Titre du document / Document title

> Increased plasma aldosterone in patients with clinical depression

> Auteur(s) / Author(s)

> EMANUELE Enzo ; GEROLDI Diego ; MINORETTI Piercarlo ; COEN Enrico ; POLITI

Pierluigi ;

> Résumé / Abstract

> Background. Clinical depression has been increasingly recognized as an

independent risk factor for adverse cardiovascular events, but the biological

mechanisms of this association remain unclear. Recent evidence for reninsystem

dysregulation in patients with depression led us to hypothesize that

aldosterone-a well-recognized contributor to vascular injury-could be increased

in depressed patients. The present study was designed, therefore, to be a

cross-sectional investigation of plasma renin and aldosterone levels in

depressed patients as compared with healthy controls with no history of

psychiatric illness. Methods. A total of 65 depressed patients and 65 age- and

gender-matched control subjects were enrolled. Following a fixed sodium and

potassium diet, venous blood samples were obtained at 9:00 a.m. to avoid the

influence of circadian rhythms. Results. Although there were no significant

differences in plasma level of renin among subjects with depression and controls

(7.9 & #8242; 5.8 vs. 6.4 & #8242; 4.3 pg/mL, respectively; p = 0.10), depressed

subjects exhibited greater mean aldosterone levels as compared with control

subjects (157.2 & #8242; 67.5 vs. 125.7 & #8242; 38.1 pg/mL, respectively; p =

0.0014). After adjusting for potential confounders, multivariate logistic

regression analysis showed that subjects with depression had 2.77 times higher

odds of elevated aldosterone levels compared with healthy control subjects (95%

confidence interval, 1.30-5.92, p = 0.008). Conclusions. Our present findings

support the hypothesis that hyperaldosteronism could be a common feature among

depressed patients, thereby suggesting that increased aldosterone levels may act

as a mediator in the pathway linking depression to unfavorable vascular events.

> Revue / Journal Title

> Archives of medical research ISSN 0188-4409

> Source / Source

> 2005, vol. 36, no5, pp. 544-548 [5 page(s) (article)]

> Langue / Language

> Anglais

>

> Editeur / Publisher

> Elsevier, New York, NY, ETATS-UNIS (1992) (Revue)

>

> Localisation / Location

> INIST-CNRS, Cote INIST : 18673, 35400013278933.0200

>

>

> Nº notice refdoc (ud4) : 17228709

>

[Guest guest]

WhAt was the salt intake of the rats ?Tiped sad Send form miiPhone ;-)May your pressure be low!CE Grim MDSpecializing in DifficultHypertension

From pubmed

Subchronic treatment with aldosterone induces depression-like behaviours and gene expression changes relevant to major depressive disorder.

Hlavacova N, Wes PD, Ondrejcakova M, Flynn ME, Poundstone PK, Babic S, Murck H, Jezova D.

SourceLaboratory of Pharmacological Neuroendocrinology, Institute of Experimental Endocrinology, Slovak Academy of Sciences, Vlarska, Bratislava, Slovakia.

Abstract

The potential role of aldosterone in the pathophysiology of depression is unclear. The aim of this study was to test the hypothesis that prolonged elevation of circulating aldosterone induces depression-like behaviour accompanied by disease-relevant changes in gene expression in the hippocampus. Subchronic (2-wk) treatment with aldosterone (2 & #956;g/100 g body weight per day) or vehicle via subcutaneous osmotic minipumps was used to induce hyperaldosteronism in male rats. All rats (n=20/treatment group) underwent a modified sucrose preference test. Half of the animals from each treatment group were exposed to the forced swim test (FST), which served both as a tool to assess depression-like behaviour and as a stress stimulus. Affymetrix microarray analysis was used to screen the entire rat genome for gene expression changes in the hippocampus. Aldosterone treatment induced an anhedonic state manifested by decreased sucrose preference. In the FST, depressogenic action of aldosterone was manifested by decreased latency to immobility and increased time spent immobile. Aldosterone treatment resulted in transcriptional changes of genes in the hippocampus involved in inflammation, glutamatergic activity, and synaptic and neuritic remodelling. Furthermore, aldosterone-regulated genes substantially overlapped with genes affected by stress in the FST. This study demonstrates the existence of a causal relationship between the hyperaldosteronism and depressive behaviour. In addition, aldosterone treatment induced changes in gene expression that may be relevant to the aetiology of major depressive disorder. Subchronic treatment with aldosterone represents a new animal model of depression, which may contribute to the development of novel targets for the treatment of depression.

>

> Titre du document / Document title

> Increased plasma aldosterone in patients with clinical depression

> Auteur(s) / Author(s)

> EMANUELE Enzo ; GEROLDI Diego ; MINORETTI Piercarlo ; COEN Enrico ; POLITI Pierluigi ;

> Résumé / Abstract

> Background. Clinical depression has been increasingly recognized as an independent risk factor for adverse cardiovascular events, but the biological mechanisms of this association remain unclear. Recent evidence for reninsystem dysregulation in patients with depression led us to hypothesize that aldosterone-a well-recognized contributor to vascular injury-could be increased in depressed patients. The present study was designed, therefore, to be a cross-sectional investigation of plasma renin and aldosterone levels in depressed patients as compared with healthy controls with no history of psychiatric illness. Methods. A total of 65 depressed patients and 65 age- and gender-matched control subjects were enrolled. Following a fixed sodium and potassium diet, venous blood samples were obtained at 9:00 a.m. to avoid the influence of circadian rhythms. Results. Although there were no significant differences in plasma level of renin among subjects with depression and controls (7.9 & #8242; 5.8 vs. 6.4 & #8242; 4.3 pg/mL, respectively; p = 0.10), depressed subjects exhibited greater mean aldosterone levels as compared with control subjects (157.2 & #8242; 67.5 vs. 125.7 & #8242; 38.1 pg/mL, respectively; p = 0.0014). After adjusting for potential confounders, multivariate logistic regression analysis showed that subjects with depression had 2.77 times higher odds of elevated aldosterone levels compared with healthy control subjects (95% confidence interval, 1.30-5.92, p = 0.008). Conclusions. Our present findings support the hypothesis that hyperaldosteronism could be a common feature among depressed patients, thereby suggesting that increased aldosterone levels may act as a mediator in the pathway linking depression to unfavorable vascular events.

> Revue / Journal Title

> Archives of medical research ISSN 0188-4409

> Source / Source

> 2005, vol. 36, no5, pp. 544-548 [5 page(s) (article)]

> Langue / Language

> Anglais

>

> Editeur / Publisher

> Elsevier, New York, NY, ETATS-UNIS (1992) (Revue)

>

> Localisation / Location

> INIST-CNRS, Cote INIST : 18673, 35400013278933.0200

>

>

> Nº notice refdoc (ud4) : 17228709

>

[Guest guest]

Would need to see full text to know this. Then it may not give this information.

> > >

> > > Titre du document / Document title

> > > Increased plasma aldosterone in patients with clinical depression

> > > Auteur(s) / Author(s)

> > > EMANUELE Enzo ; GEROLDI Diego ; MINORETTI Piercarlo ; COEN Enrico ; POLITI

Pierluigi ;

> > > Résumé / Abstract

> > > Background. Clinical depression has been increasingly recognized as an

independent risk factor for adverse cardiovascular events, but the biological

mechanisms of this association remain unclear. Recent evidence for reninsystem

dysregulation in patients with depression led us to hypothesize that

aldosterone-a well-recognized contributor to vascular injury-could be increased

in depressed patients. The present study was designed, therefore, to be a

cross-sectional investigation of plasma renin and aldosterone levels in

depressed patients as compared with healthy controls with no history of

psychiatric illness. Methods. A total of 65 depressed patients and 65 age- and

gender-matched control subjects were enrolled. Following a fixed sodium and

potassium diet, venous blood samples were obtained at 9:00 a.m. to avoid the

influence of circadian rhythms. Results. Although there were no significant

differences in plasma level of renin among subjects with depression and controls

(7.9 & #8242; 5.8 vs. 6.4 & #8242; 4.3 pg/mL, respectively; p = 0.10), depressed

subjects exhibited greater mean aldosterone levels as compared with control

subjects (157.2 & #8242; 67.5 vs. 125.7 & #8242; 38.1 pg/mL, respectively; p =

0.0014). After adjusting for potential confounders, multivariate logistic

regression analysis showed that subjects with depression had 2.77 times higher

odds of elevated aldosterone levels compared with healthy control subjects (95%

confidence interval, 1.30-5.92, p = 0.008). Conclusions. Our present findings

support the hypothesis that hyperaldosteronism could be a common feature among

depressed patients, thereby suggesting that increased aldosterone levels may act

as a mediator in the pathway linking depression to unfavorable vascular events.

> > > Revue / Journal Title

> > > Archives of medical research ISSN 0188-4409

> > > Source / Source

> > > 2005, vol. 36, no5, pp. 544-548 [5 page(s) (article)]

> > > Langue / Language

> > > Anglais

> > >

> > > Editeur / Publisher

> > > Elsevier, New York, NY, ETATS-UNIS (1992) (Revue)

> > >

> > > Localisation / Location

> > > INIST-CNRS, Cote INIST : 18673, 35400013278933.0200

> > >

> > >

> > > Nº notice refdoc (ud4) : 17228709

> > >

> >

> >

>

[Guest guest]

Thie info looks kind of slim to me,2 articles in 1992 and a 7 person study in

2003. Would think there would be more interest and activity if there was merit!

I may learn more when Dr. Bolton snawers my Spiro question. Thanks.

- 64 yo morb. ob. male - 12mm X 13mm rt. a.adnoma with previous rt. flank &

testicle pain. I have decided against an adrenalectomy at this time since

Meds. are working so well. Current BP: 130/77

Other Issues/Opportunities: COPD w/ft Oxygen, OSA w Bi-Pap settings 13/19, DM2.

and PTSD

Meds: Duloxetine hcl 80 MG, Mirtazapine 15 MG, Metoprolol Tartrate 200 MG,

Metformin 2000MG and Spironolactone 75 MG.

> > > >

> > > > Titre du document / Document title

> > > > Increased plasma aldosterone in patients with clinical depression

> > > > Auteur(s) / Author(s)

> > > > EMANUELE Enzo ; GEROLDI Diego ; MINORETTI Piercarlo ; COEN Enrico ;

POLITI Pierluigi ;

> > > > Résumé / Abstract

> > > > Background. Clinical depression has been increasingly recognized as an

independent risk factor for adverse cardiovascular events, but the biological

mechanisms of this association remain unclear. Recent evidence for reninsystem

dysregulation in patients with depression led us to hypothesize that

aldosterone-a well-recognized contributor to vascular injury-could be increased

in depressed patients. The present study was designed, therefore, to be a

cross-sectional investigation of plasma renin and aldosterone levels in

depressed patients as compared with healthy controls with no history of

psychiatric illness. Methods. A total of 65 depressed patients and 65 age- and

gender-matched control subjects were enrolled. Following a fixed sodium and

potassium diet, venous blood samples were obtained at 9:00 a.m. to avoid the

influence of circadian rhythms. Results. Although there were no significant

differences in plasma level of renin among subjects with depression and controls

(7.9 & #8242; 5.8 vs. 6.4 & #8242; 4.3 pg/mL, respectively; p = 0.10), depressed

subjects exhibited greater mean aldosterone levels as compared with control

subjects (157.2 & #8242; 67.5 vs. 125.7 & #8242; 38.1 pg/mL, respectively; p =

0.0014). After adjusting for potential confounders, multivariate logistic

regression analysis showed that subjects with depression had 2.77 times higher

odds of elevated aldosterone levels compared with healthy control subjects (95%

confidence interval, 1.30-5.92, p = 0.008). Conclusions. Our present findings

support the hypothesis that hyperaldosteronism could be a common feature among

depressed patients, thereby suggesting that increased aldosterone levels may act

as a mediator in the pathway linking depression to unfavorable vascular events.

> > > > Revue / Journal Title

> > > > Archives of medical research ISSN 0188-4409

> > > > Source / Source

> > > > 2005, vol. 36, no5, pp. 544-548 [5 page(s) (article)]

> > > > Langue / Language

> > > > Anglais

> > > >

> > > > Editeur / Publisher

> > > > Elsevier, New York, NY, ETATS-UNIS (1992) (Revue)

> > > >

> > > > Localisation / Location

> > > > INIST-CNRS, Cote INIST : 18673, 35400013278933.0200

> > > >

> > > >

> > > > Nº notice refdoc (ud4) : 17228709

> > > >

> > >

> > >

> >

>

[Guest guest]

Often you can get the complete article if it is this old. So go to pubmed and see if it has free access now.CE Grim MDOn Jul 24, 2011, at 1:30 PM, Francis Bill SUSPECTED PA wrote: Would need to see full text to know this. Then it may not give this information. > > > > > > Titre du document / Document title > > > Increased plasma aldosterone in patients with clinical depression > > > Auteur(s) / Author(s) > > > EMANUELE Enzo ; GEROLDI Diego ; MINORETTI Piercarlo ; COEN Enrico ; POLITI Pierluigi ; > > > Résumé / Abstract > > > Background. Clinical depression has been increasingly recognized as an independent risk factor for adverse cardiovascular events, but the biological mechanisms of this association remain unclear. Recent evidence for reninsystem dysregulation in patients with depression led us to hypothesize that aldosterone-a well-recognized contributor to vascular injury-could be increased in depressed patients. The present study was designed, therefore, to be a cross-sectional investigation of plasma renin and aldosterone levels in depressed patients as compared with healthy controls with no history of psychiatric illness. Methods. A total of 65 depressed patients and 65 age- and gender-matched control subjects were enrolled. Following a fixed sodium and potassium diet, venous blood samples were obtained at 9:00 a.m. to avoid the influence of circadian rhythms. Results. Although there were no significant differences in plasma level of renin among subjects with depression and controls (7.9 & #8242; 5.8 vs. 6.4 & #8242; 4.3 pg/mL, respectively; p = 0.10), depressed subjects exhibited greater mean aldosterone levels as compared with control subjects (157.2 & #8242; 67.5 vs. 125.7 & #8242; 38.1 pg/mL, respectively; p = 0.0014). After adjusting for potential confounders, multivariate logistic regression analysis showed that subjects with depression had 2.77 times higher odds of elevated aldosterone levels compared with healthy control subjects (95% confidence interval, 1.30-5.92, p = 0.008). Conclusions. Our present findings support the hypothesis that hyperaldosteronism could be a common feature among depressed patients, thereby suggesting that increased aldosterone levels may act as a mediator in the pathway linking depression to unfavorable vascular events. > > > Revue / Journal Title > > > Archives of medical research ISSN 0188-4409 > > > Source / Source > > > 2005, vol. 36, no5, pp. 544-548 [5 page(s) (article)] > > > Langue / Language > > > Anglais > > > > > > Editeur / Publisher > > > Elsevier, New York, NY, ETATS-UNIS (1992) (Revue) > > > > > > Localisation / Location > > > INIST-CNRS, Cote INIST : 18673, 35400013278933.0200 > > > > > > > > > Nº notice refdoc (ud4) : 17228709 > > > > > > > >

[Guest guest]

Agree if it was good data it would have been followed up. You can search the author's name in pubmed and see what they have published since.CE Grim MD Thie info looks kind of slim to me,2 articles in 1992 and a 7 person study in 2003. Would think there would be more interest and activity if there was merit! I may learn more when Dr. Bolton snawers my Spiro question. Thanks. - 64 yo morb. ob. male - 12mm X 13mm rt. a.adnoma with previous rt. flank & testicle pain. I have decided against an adrenalectomy at this time since Meds. are working so well. Current BP: 130/77 Other Issues/Opportunities: COPD w/ft Oxygen, OSA w Bi-Pap settings 13/19, DM2. and PTSD Meds: Duloxetine hcl 80 MG, Mirtazapine 15 MG, Metoprolol Tartrate 200 MG, Metformin 2000MG and Spironolactone 75 MG. > > > > > > > > Titre du document / Document title > > > > Increased plasma aldosterone in patients with clinical depression > > > > Auteur(s) / Author(s) > > > > EMANUELE Enzo ; GEROLDI Diego ; MINORETTI Piercarlo ; COEN Enrico ; POLITI Pierluigi ; > > > > Résumé / Abstract > > > > Background. Clinical depression has been increasingly recognized as an independent risk factor for adverse cardiovascular events, but the biological mechanisms of this association remain unclear. Recent evidence for reninsystem dysregulation in patients with depression led us to hypothesize that aldosterone-a well-recognized contributor to vascular injury-could be increased in depressed patients. The present study was designed, therefore, to be a cross-sectional investigation of plasma renin and aldosterone levels in depressed patients as compared with healthy controls with no history of psychiatric illness. Methods. A total of 65 depressed patients and 65 age- and gender-matched control subjects were enrolled. Following a fixed sodium and potassium diet, venous blood samples were obtained at 9:00 a.m. to avoid the influence of circadian rhythms. Results. Although there were no significant differences in plasma level of renin among subjects with depression and controls (7.9 & #8242; 5.8 vs. 6.4 & #8242; 4.3 pg/mL, respectively; p = 0.10), depressed subjects exhibited greater mean aldosterone levels as compared with control subjects (157.2 & #8242; 67.5 vs. 125.7 & #8242; 38.1 pg/mL, respectively; p = 0.0014). After adjusting for potential confounders, multivariate logistic regression analysis showed that subjects with depression had 2.77 times higher odds of elevated aldosterone levels compared with healthy control subjects (95% confidence interval, 1.30-5.92, p = 0.008). Conclusions. Our present findings support the hypothesis that hyperaldosteronism could be a common feature among depressed patients, thereby suggesting that increased aldosterone levels may act as a mediator in the pathway linking depression to unfavorable vascular events. > > > > Revue / Journal Title > > > > Archives of medical research ISSN 0188-4409 > > > > Source / Source > > > > 2005, vol. 36, no5, pp. 544-548 [5 page(s) (article)] > > > > Langue / Language > > > > Anglais > > > > > > > > Editeur / Publisher > > > > Elsevier, New York, NY, ETATS-UNIS (1992) (Revue) > > > > > > > > Localisation / Location > > > > INIST-CNRS, Cote INIST : 18673, 35400013278933.0200 > > > > > > > > > > > > Nº notice refdoc (ud4) : 17228709 > > > > > > > > > > > > >

[Guest guest]

looks like you have to pay $45 to get full text.

> > > > >

> > > > > Titre du document / Document title

> > > > > Increased plasma aldosterone in patients with clinical

> > depression

> > > > > Auteur(s) / Author(s)

> > > > > EMANUELE Enzo ; GEROLDI Diego ; MINORETTI Piercarlo ; COEN

> > Enrico ; POLITI Pierluigi ;

> > > > > Résumé / Abstract

> > > > > Background. Clinical depression has been increasingly

> > recognized as an independent risk factor for adverse cardiovascular

> > events, but the biological mechanisms of this association remain

> > unclear. Recent evidence for reninsystem dysregulation in patients

> > with depression led us to hypothesize that aldosterone-a well-

> > recognized contributor to vascular injury-could be increased in

> > depressed patients. The present study was designed, therefore, to be

> > a cross-sectional investigation of plasma renin and aldosterone

> > levels in depressed patients as compared with healthy controls with

> > no history of psychiatric illness. Methods. A total of 65 depressed

> > patients and 65 age- and gender-matched control subjects were

> > enrolled. Following a fixed sodium and potassium diet, venous blood

> > samples were obtained at 9:00 a.m. to avoid the influence of

> > circadian rhythms. Results. Although there were no significant

> > differences in plasma level of renin among subjects with depression

> > and controls (7.9 & #8242; 5.8 vs. 6.4 & #8242; 4.3 pg/mL,

> > respectively; p = 0.10), depressed subjects exhibited greater mean

> > aldosterone levels as compared with control subjects (157.2 & #8242;

> > 67.5 vs. 125.7 & #8242; 38.1 pg/mL, respectively; p = 0.0014). After

> > adjusting for potential confounders, multivariate logistic

> > regression analysis showed that subjects with depression had 2.77

> > times higher odds of elevated aldosterone levels compared with

> > healthy control subjects (95% confidence interval, 1.30-5.92, p =

> > 0.008). Conclusions. Our present findings support the hypothesis

> > that hyperaldosteronism could be a common feature among depressed

> > patients, thereby suggesting that increased aldosterone levels may

> > act as a mediator in the pathway linking depression to unfavorable

> > vascular events.

> > > > > Revue / Journal Title

> > > > > Archives of medical research ISSN 0188-4409

> > > > > Source / Source

> > > > > 2005, vol. 36, no5, pp. 544-548 [5 page(s) (article)]

> > > > > Langue / Language

> > > > > Anglais

> > > > >

> > > > > Editeur / Publisher

> > > > > Elsevier, New York, NY, ETATS-UNIS (1992) (Revue)

> > > > >

> > > > > Localisation / Location

> > > > > INIST-CNRS, Cote INIST : 18673, 35400013278933.0200

> > > > >

> > > > >

> > > > > Nº notice refdoc (ud4) : 17228709

> > > > >

> > > >

> > > >

> > >

> >

> >

>

[Guest guest]

I would wait unless we have someone here who has a faculty appointment and can get this. Tiped sad Send form miiPhone ;-)May your pressure be low!CE Grim MDSpecializing in DifficultHypertension

looks like you have to pay $45 to get full text.

> > > > >

> > > > > Titre du document / Document title

> > > > > Increased plasma aldosterone in patients with clinical

> > depression

> > > > > Auteur(s) / Author(s)

> > > > > EMANUELE Enzo ; GEROLDI Diego ; MINORETTI Piercarlo ; COEN

> > Enrico ; POLITI Pierluigi ;

> > > > > Résumé / Abstract

> > > > > Background. Clinical depression has been increasingly

> > recognized as an independent risk factor for adverse cardiovascular

> > events, but the biological mechanisms of this association remain

> > unclear. Recent evidence for reninsystem dysregulation in patients

> > with depression led us to hypothesize that aldosterone-a well-

> > recognized contributor to vascular injury-could be increased in

> > depressed patients. The present study was designed, therefore, to be

> > a cross-sectional investigation of plasma renin and aldosterone

> > levels in depressed patients as compared with healthy controls with

> > no history of psychiatric illness. Methods. A total of 65 depressed

> > patients and 65 age- and gender-matched control subjects were

> > enrolled. Following a fixed sodium and potassium diet, venous blood

> > samples were obtained at 9:00 a.m. to avoid the influence of

> > circadian rhythms. Results. Although there were no significant

> > differences in plasma level of renin among subjects with depression

> > and controls (7.9 & #8242; 5.8 vs. 6.4 & #8242; 4.3 pg/mL,

> > respectively; p = 0.10), depressed subjects exhibited greater mean

> > aldosterone levels as compared with control subjects (157.2 & #8242;

> > 67.5 vs. 125.7 & #8242; 38.1 pg/mL, respectively; p = 0.0014). After

> > adjusting for potential confounders, multivariate logistic

> > regression analysis showed that subjects with depression had 2.77

> > times higher odds of elevated aldosterone levels compared with

> > healthy control subjects (95% confidence interval, 1.30-5.92, p =

> > 0.008). Conclusions. Our present findings support the hypothesis

> > that hyperaldosteronism could be a common feature among depressed

> > patients, thereby suggesting that increased aldosterone levels may

> > act as a mediator in the pathway linking depression to unfavorable

> > vascular events.

> > > > > Revue / Journal Title

> > > > > Archives of medical research ISSN 0188-4409

> > > > > Source / Source

> > > > > 2005, vol. 36, no5, pp. 544-548 [5 page(s) (article)]

> > > > > Langue / Language

> > > > > Anglais

> > > > >

> > > > > Editeur / Publisher

> > > > > Elsevier, New York, NY, ETATS-UNIS (1992) (Revue)

> > > > >

> > > > > Localisation / Location

> > > > > INIST-CNRS, Cote INIST : 18673, 35400013278933.0200

> > > > >

> > > > >

> > > > > Nº notice refdoc (ud4) : 17228709

> > > > >

> > > >

> > > >

> > >

> >

> >

>

[Guest guest]

I vote to save our money, look at the conclusion again: " ...FINDINGS

SUPPORT...COULD BE...THEREBY SUGGESTING...MAY ACT! They didn't find anything

other than how to make $45! Thanks for looking and there may be something to it

but it needs alot more validating and a concrete conclusion for me to pay

attention!

Our present findings support the hypothesis

> > that hyperaldosteronism could be a common feature among depressed

> > patients, thereby suggesting that increased aldosterone levels may

> > act as a mediator in the pathway linking depression to unfavorable

> > vascular events.

- 64 yo morb. ob. male - 12mm X 13mm rt. a.adnoma with previous rt. flank &

testicle pain. I have decided against an adrenalectomy at this time since

Meds. are working so well. Current BP: 130/77

Other Issues/Opportunities: COPD w/ft Oxygen, OSA w Bi-Pap settings 13/19, DM2.

and PTSD

Meds: Duloxetine hcl 80 MG, Mirtazapine 15 MG, Metoprolol Tartrate 200 MG,

Metformin 2000MG and Spironolactone 75 MG.

> > > > > >

> > > > > > Titre du document / Document title

> > > > > > Increased plasma aldosterone in patients with clinical

> > > depression

> > > > > > Auteur(s) / Author(s)

> > > > > > EMANUELE Enzo ; GEROLDI Diego ; MINORETTI Piercarlo ; COEN

> > > Enrico ; POLITI Pierluigi ;

> > > > > > Résumé / Abstract

> > > > > > Background. Clinical depression has been increasingly

> > > recognized as an independent risk factor for adverse cardiovascular

> > > events, but the biological mechanisms of this association remain

> > > unclear. Recent evidence for reninsystem dysregulation in patients

> > > with depression led us to hypothesize that aldosterone-a well-

> > > recognized contributor to vascular injury-could be increased in

> > > depressed patients. The present study was designed, therefore, to be

> > > a cross-sectional investigation of plasma renin and aldosterone

> > > levels in depressed patients as compared with healthy controls with

> > > no history of psychiatric illness. Methods. A total of 65 depressed

> > > patients and 65 age- and gender-matched control subjects were

> > > enrolled. Following a fixed sodium and potassium diet, venous blood

> > > samples were obtained at 9:00 a.m. to avoid the influence of

> > > circadian rhythms. Results. Although there were no significant

> > > differences in plasma level of renin among subjects with depression

> > > and controls (7.9 & #8242; 5.8 vs. 6.4 & #8242; 4.3 pg/mL,

> > > respectively; p = 0.10), depressed subjects exhibited greater mean

> > > aldosterone levels as compared with control subjects (157.2 & #8242;

> > > 67.5 vs. 125.7 & #8242; 38.1 pg/mL, respectively; p = 0.0014). After

> > > adjusting for potential confounders, multivariate logistic

> > > regression analysis showed that subjects with depression had 2.77

> > > times higher odds of elevated aldosterone levels compared with

> > > healthy control subjects (95% confidence interval, 1.30-5.92, p =

> > > 0.008). Conclusions. Our present findings support the hypothesis

> > > that hyperaldosteronism could be a common feature among depressed

> > > patients, thereby suggesting that increased aldosterone levels may

> > > act as a mediator in the pathway linking depression to unfavorable

> > > vascular events.

> > > > > > Revue / Journal Title

> > > > > > Archives of medical research ISSN 0188-4409

> > > > > > Source / Source

> > > > > > 2005, vol. 36, no5, pp. 544-548 [5 page(s) (article)]

> > > > > > Langue / Language

> > > > > > Anglais

> > > > > >

> > > > > > Editeur / Publisher

> > > > > > Elsevier, New York, NY, ETATS-UNIS (1992) (Revue)

> > > > > >

> > > > > > Localisation / Location

> > > > > > INIST-CNRS, Cote INIST : 18673, 35400013278933.0200

> > > > > >

> > > > > >

> > > > > > Nº notice refdoc (ud4) : 17228709

> > > > > >

> > > > >

> > > > >

> > > >

> > >

> > >

> >

>

[Guest guest]

I'll try tomorrow to get it

looks like you have to pay $45 to get full text.> > > > >> > > > > Titre du document / Document title> > > > > Increased plasma aldosterone in patients with clinical > > depression> > > > > Auteur(s) / Author(s)> > > > > EMANUELE Enzo ; GEROLDI Diego ; MINORETTI Piercarlo ; COEN > > Enrico ; POLITI Pierluigi ;> > > > > Résumé / Abstract> > > > > Background. Clinical depression has been increasingly

> > recognized as an independent risk factor for adverse cardiovascular > > events, but the biological mechanisms of this association remain > > unclear. Recent evidence for reninsystem dysregulation in patients > > with depression led us to hypothesize that aldosterone-a well- > > recognized contributor to vascular injury-could be increased in > > depressed patients. The present study was designed, therefore, to be > > a cross-sectional investigation of plasma renin and aldosterone > > levels in depressed patients as compared with healthy controls with > > no history of psychiatric illness. Methods. A total of 65 depressed > > patients and 65 age- and gender-matched control subjects were > > enrolled. Following a fixed sodium and potassium diet, venous blood > > samples were obtained at 9:00 a.m. to avoid the influence of >

> circadian rhythms. Results. Although there were no significant > > differences in plasma level of renin among subjects with depression > > and controls (7.9 & #8242; 5.8 vs. 6.4 & #8242; 4.3 pg/mL, > > respectively; p = 0.10), depressed subjects exhibited greater mean > > aldosterone levels as compared with control subjects (157.2 & #8242; > > 67.5 vs. 125.7 & #8242; 38.1 pg/mL, respectively; p = 0.0014). After > > adjusting for potential confounders, multivariate logistic > > regression analysis showed that subjects with depression had 2.77 > > times higher odds of elevated aldosterone levels compared with > > healthy control subjects (95% confidence interval, 1.30-5.92, p = > > 0.008). Conclusions. Our present findings support the hypothesis > > that hyperaldosteronism could be a common feature among depressed > >

patients, thereby suggesting that increased aldosterone levels may > > act as a mediator in the pathway linking depression to unfavorable > > vascular events.> > > > > Revue / Journal Title> > > > > Archives of medical research ISSN 0188-4409> > > > > Source / Source> > > > > 2005, vol. 36, no5, pp. 544-548 [5 page(s) (article)]> > > > > Langue / Language> > > > > Anglais> > > > >> > > > > Editeur / Publisher> > > > > Elsevier, New York, NY, ETATS-UNIS (1992) (Revue)> > > > >> > > > > Localisation / Location> > > > > INIST-CNRS, Cote INIST : 18673, 35400013278933.0200> > > > >> > > > >> > > > > Nº notice refdoc (ud4) : 17228709> > > >

>> > > >> > > >> > >> >> >>

[Guest guest]

There are many it this group that have mental health problems. It would be

interesting to know if the percentage is higher then normal.

All studies seem to be suggesting the cause and effect.

> > > > > > >

> > > > > > > Titre du document / Document title

> > > > > > > Increased plasma aldosterone in patients with clinical

> > > > depression

> > > > > > > Auteur(s) / Author(s)

> > > > > > > EMANUELE Enzo ; GEROLDI Diego ; MINORETTI Piercarlo ; COEN

> > > > Enrico ; POLITI Pierluigi ;

> > > > > > > Résumé / Abstract

> > > > > > > Background. Clinical depression has been increasingly

> > > > recognized as an independent risk factor for adverse cardiovascular

> > > > events, but the biological mechanisms of this association remain

> > > > unclear. Recent evidence for reninsystem dysregulation in patients

> > > > with depression led us to hypothesize that aldosterone-a well-

> > > > recognized contributor to vascular injury-could be increased in

> > > > depressed patients. The present study was designed, therefore, to be

> > > > a cross-sectional investigation of plasma renin and aldosterone

> > > > levels in depressed patients as compared with healthy controls with

> > > > no history of psychiatric illness. Methods. A total of 65 depressed

> > > > patients and 65 age- and gender-matched control subjects were

> > > > enrolled. Following a fixed sodium and potassium diet, venous blood

> > > > samples were obtained at 9:00 a.m. to avoid the influence of

> > > > circadian rhythms. Results. Although there were no significant

> > > > differences in plasma level of renin among subjects with depression

> > > > and controls (7.9 & #8242; 5.8 vs. 6.4 & #8242; 4.3 pg/mL,

> > > > respectively; p = 0.10), depressed subjects exhibited greater mean

> > > > aldosterone levels as compared with control subjects (157.2 & #8242;

> > > > 67.5 vs. 125.7 & #8242; 38.1 pg/mL, respectively; p = 0.0014). After

> > > > adjusting for potential confounders, multivariate logistic

> > > > regression analysis showed that subjects with depression had 2.77

> > > > times higher odds of elevated aldosterone levels compared with

> > > > healthy control subjects (95% confidence interval, 1.30-5.92, p =

> > > > 0.008). Conclusions. Our present findings support the hypothesis

> > > > that hyperaldosteronism could be a common feature among depressed

> > > > patients, thereby suggesting that increased aldosterone levels may

> > > > act as a mediator in the pathway linking depression to unfavorable

> > > > vascular events.

> > > > > > > Revue / Journal Title

> > > > > > > Archives of medical research ISSN 0188-4409

> > > > > > > Source / Source

> > > > > > > 2005, vol. 36, no5, pp. 544-548 [5 page(s) (article)]

> > > > > > > Langue / Language

> > > > > > > Anglais

> > > > > > >

> > > > > > > Editeur / Publisher

> > > > > > > Elsevier, New York, NY, ETATS-UNIS (1992) (Revue)

> > > > > > >

> > > > > > > Localisation / Location

> > > > > > > INIST-CNRS, Cote INIST : 18673, 35400013278933.0200

> > > > > > >

> > > > > > >

> > > > > > > Nº notice refdoc (ud4) : 17228709

> > > > > > >

> > > > > >

> > > > > >

> > > > >

> > > >

> > > >

> > >

> >

>

[Guest guest]

The runaround that most of us have been given by the medical professionals,

combined with the side effects of many of the drugs we have been prescribed, is

in my opinion in and of itself enough to cause or exacerbate depression,

anxiety, etc!

> > > > > > > >

> > > > > > > > Titre du document / Document title

> > > > > > > > Increased plasma aldosterone in patients with clinical

> > > > > depression

> > > > > > > > Auteur(s) / Author(s)

> > > > > > > > EMANUELE Enzo ; GEROLDI Diego ; MINORETTI Piercarlo ; COEN

> > > > > Enrico ; POLITI Pierluigi ;

> > > > > > > > Résumé / Abstract

> > > > > > > > Background. Clinical depression has been increasingly

> > > > > recognized as an independent risk factor for adverse cardiovascular

> > > > > events, but the biological mechanisms of this association remain

> > > > > unclear. Recent evidence for reninsystem dysregulation in patients

> > > > > with depression led us to hypothesize that aldosterone-a well-

> > > > > recognized contributor to vascular injury-could be increased in

> > > > > depressed patients. The present study was designed, therefore, to be

> > > > > a cross-sectional investigation of plasma renin and aldosterone

> > > > > levels in depressed patients as compared with healthy controls with

> > > > > no history of psychiatric illness. Methods. A total of 65 depressed

> > > > > patients and 65 age- and gender-matched control subjects were

> > > > > enrolled. Following a fixed sodium and potassium diet, venous blood

> > > > > samples were obtained at 9:00 a.m. to avoid the influence of

> > > > > circadian rhythms. Results. Although there were no significant

> > > > > differences in plasma level of renin among subjects with depression

> > > > > and controls (7.9 & #8242; 5.8 vs. 6.4 & #8242; 4.3 pg/mL,

> > > > > respectively; p = 0.10), depressed subjects exhibited greater mean

> > > > > aldosterone levels as compared with control subjects (157.2 & #8242;

> > > > > 67.5 vs. 125.7 & #8242; 38.1 pg/mL, respectively; p = 0.0014). After

> > > > > adjusting for potential confounders, multivariate logistic

> > > > > regression analysis showed that subjects with depression had 2.77

> > > > > times higher odds of elevated aldosterone levels compared with

> > > > > healthy control subjects (95% confidence interval, 1.30-5.92, p =

> > > > > 0.008). Conclusions. Our present findings support the hypothesis

> > > > > that hyperaldosteronism could be a common feature among depressed

> > > > > patients, thereby suggesting that increased aldosterone levels may

> > > > > act as a mediator in the pathway linking depression to unfavorable

> > > > > vascular events.

> > > > > > > > Revue / Journal Title

> > > > > > > > Archives of medical research ISSN 0188-4409

> > > > > > > > Source / Source

> > > > > > > > 2005, vol. 36, no5, pp. 544-548 [5 page(s) (article)]

> > > > > > > > Langue / Language

> > > > > > > > Anglais

> > > > > > > >

> > > > > > > > Editeur / Publisher

> > > > > > > > Elsevier, New York, NY, ETATS-UNIS (1992) (Revue)

> > > > > > > >

> > > > > > > > Localisation / Location

> > > > > > > > INIST-CNRS, Cote INIST : 18673, 35400013278933.0200

> > > > > > > >

> > > > > > > >

> > > > > > > > Nº notice refdoc (ud4) : 17228709

> > > > > > > >

> > > > > > >

> > > > > > >

> > > > > >

> > > > >

> > > > >

> > > >

> > >

> >

>

[Guest guest]

I prefer the term "emotional health" problems as "mental health" seems to imply an organic disorder that is permanent. And sometimes it is "iatrogenic" - physician (or any medical professional) caused. I used to lecture on this when I was on the faculty in Oklahoma at State University in terms of paramedics, wherein medics are viewed as "lifesavers" by the general public, when in truth rarely did we truly save a life, but we impacted every life we came in contact with every day - so even for mere minutes with a patient it only took ONE single incident of rudeness, overt arrogance, or some negative moment and THAT is what the patient remembered forever and that one moment ruined any and all good work done in the past for that patient. It's like a 10:1 ratio - 1 single bad moment can easily, 10 times, overshadow 10 good

moments in the patients memory. It's the same for all of us. We've had many a good experience (or "normal" experience we could say) visiting the doctor, but one (and for most there were not just one) bad experience overshadows the rest.

Like fast food too.....eat 100 burgers at a place just fine, but get one bad one and it's pretty hard to ever go back. I wish medical professionals would get this concept that they ethically, are there to serve the patient (within reason of course), and the patient isn't there just for them.

Subject: Re: depression and adverse cardiovascular eventsTo: hyperaldosteronism Date: Monday, July 25, 2011, 9:24 AM

The runaround that most of us have been given by the medical professionals, combined with the side effects of many of the drugs we have been prescribed, is in my opinion in and of itself enough to cause or exacerbate depression, anxiety, etc!> > > > > > > >> > > > > > > > Titre du document / Document title> > > > > > > > Increased plasma aldosterone in patients with clinical > > > > > depression> > >

> > > > > Auteur(s) / Author(s)> > > > > > > > EMANUELE Enzo ; GEROLDI Diego ; MINORETTI Piercarlo ; COEN > > > > > Enrico ; POLITI Pierluigi ;> > > > > > > > Résumé / Abstract> > > > > > > > Background. Clinical depression has been increasingly > > > > > recognized as an independent risk factor for adverse cardiovascular > > > > > events, but the biological mechanisms of this association remain > > > > > unclear. Recent evidence for reninsystem dysregulation in patients > > > > > with depression led us to hypothesize that aldosterone-a well- > > > > > recognized contributor to vascular injury-could be increased in > > > > > depressed patients. The present study was designed, therefore, to be > > > >

> a cross-sectional investigation of plasma renin and aldosterone > > > > > levels in depressed patients as compared with healthy controls with > > > > > no history of psychiatric illness. Methods. A total of 65 depressed > > > > > patients and 65 age- and gender-matched control subjects were > > > > > enrolled. Following a fixed sodium and potassium diet, venous blood > > > > > samples were obtained at 9:00 a.m. to avoid the influence of > > > > > circadian rhythms. Results. Although there were no significant > > > > > differences in plasma level of renin among subjects with depression > > > > > and controls (7.9 & #8242; 5.8 vs. 6.4 & #8242; 4.3 pg/mL, > > > > > respectively; p = 0.10), depressed subjects exhibited greater mean > > > > > aldosterone levels

as compared with control subjects (157.2 & #8242; > > > > > 67.5 vs. 125.7 & #8242; 38.1 pg/mL, respectively; p = 0.0014). After > > > > > adjusting for potential confounders, multivariate logistic > > > > > regression analysis showed that subjects with depression had 2.77 > > > > > times higher odds of elevated aldosterone levels compared with > > > > > healthy control subjects (95% confidence interval, 1.30-5.92, p = > > > > > 0.008). Conclusions. Our present findings support the hypothesis > > > > > that hyperaldosteronism could be a common feature among depressed > > > > > patients, thereby suggesting that increased aldosterone levels may > > > > > act as a mediator in the pathway linking depression to unfavorable > > > > > vascular events.> >

> > > > > > Revue / Journal Title> > > > > > > > Archives of medical research ISSN 0188-4409> > > > > > > > Source / Source> > > > > > > > 2005, vol. 36, no5, pp. 544-548 [5 page(s) (article)]> > > > > > > > Langue / Language> > > > > > > > Anglais> > > > > > > >> > > > > > > > Editeur / Publisher> > > > > > > > Elsevier, New York, NY, ETATS-UNIS (1992) (Revue)> > > > > > > >> > > > > > > > Localisation / Location> > > > > > > > INIST-CNRS, Cote INIST : 18673, 35400013278933.0200> > > > > > > >> > > > > > > >> > > > > > > > Nº notice refdoc (ud4) :

17228709> > > > > > > >> > > > > > >> > > > > > >> > > > > >> > > > >> > > > >> > > >> > >> >>

[Guest guest]

It is important too in research not to assume it's cause and effect only, but that many a medical condition may exacerbate something that already exists. In other words it made a tendency for depression worse - served as a trigger - but didn't cause it per se. That's just research, being willing to take the results where ever they lead one to

Subject: Re: depression and adverse cardiovascular eventsTo: hyperaldosteronism Date: Monday, July 25, 2011, 7:14 AM

There are many it this group that have mental health problems. It would be interesting to know if the percentage is higher then normal. All studies seem to be suggesting the cause and effect. > > > > > > >> > > > > > > Titre du document / Document title> > > > > > > Increased plasma aldosterone in patients with clinical > > > > depression> > > > > > > Auteur(s) / Author(s)> > > > > > > EMANUELE Enzo ; GEROLDI Diego ; MINORETTI Piercarlo ; COEN >

> > > Enrico ; POLITI Pierluigi ;> > > > > > > Résumé / Abstract> > > > > > > Background. Clinical depression has been increasingly > > > > recognized as an independent risk factor for adverse cardiovascular > > > > events, but the biological mechanisms of this association remain > > > > unclear. Recent evidence for reninsystem dysregulation in patients > > > > with depression led us to hypothesize that aldosterone-a well- > > > > recognized contributor to vascular injury-could be increased in > > > > depressed patients. The present study was designed, therefore, to be > > > > a cross-sectional investigation of plasma renin and aldosterone > > > > levels in depressed patients as compared with healthy controls with > > > > no history of psychiatric

illness. Methods. A total of 65 depressed > > > > patients and 65 age- and gender-matched control subjects were > > > > enrolled. Following a fixed sodium and potassium diet, venous blood > > > > samples were obtained at 9:00 a.m. to avoid the influence of > > > > circadian rhythms. Results. Although there were no significant > > > > differences in plasma level of renin among subjects with depression > > > > and controls (7.9 & #8242; 5.8 vs. 6.4 & #8242; 4.3 pg/mL, > > > > respectively; p = 0.10), depressed subjects exhibited greater mean > > > > aldosterone levels as compared with control subjects (157.2 & #8242; > > > > 67.5 vs. 125.7 & #8242; 38.1 pg/mL, respectively; p = 0.0014). After > > > > adjusting for potential confounders, multivariate logistic > > > >

regression analysis showed that subjects with depression had 2.77 > > > > times higher odds of elevated aldosterone levels compared with > > > > healthy control subjects (95% confidence interval, 1.30-5.92, p = > > > > 0.008). Conclusions. Our present findings support the hypothesis > > > > that hyperaldosteronism could be a common feature among depressed > > > > patients, thereby suggesting that increased aldosterone levels may > > > > act as a mediator in the pathway linking depression to unfavorable > > > > vascular events.> > > > > > > Revue / Journal Title> > > > > > > Archives of medical research ISSN 0188-4409> > > > > > > Source / Source> > > > > > > 2005, vol. 36, no5, pp. 544-548 [5 page(s) (article)]> > > > > >

> Langue / Language> > > > > > > Anglais> > > > > > >> > > > > > > Editeur / Publisher> > > > > > > Elsevier, New York, NY, ETATS-UNIS (1992) (Revue)> > > > > > >> > > > > > > Localisation / Location> > > > > > > INIST-CNRS, Cote INIST : 18673, 35400013278933.0200> > > > > > >> > > > > > >> > > > > > > Nº notice refdoc (ud4) : 17228709> > > > > > >> > > > > >> > > > > >> > > > >> > > >> > > >> > >> >>

[Guest guest]

I was taught the sick never inconvenience the well. Tiped sad Send form miiPhone ;-)May your pressure be low!CE Grim MDSpecializing in DifficultHypertension

I prefer the term "emotional health" problems as "mental health" seems to imply an organic disorder that is permanent. And sometimes it is "iatrogenic" - physician (or any medical professional) caused. I used to lecture on this when I was on the faculty in Oklahoma at State University in terms of paramedics, wherein medics are viewed as "lifesavers" by the general public, when in truth rarely did we truly save a life, but we impacted every life we came in contact with every day - so even for mere minutes with a patient it only took ONE single incident of rudeness, overt arrogance, or some negative moment and THAT is what the patient remembered forever and that one moment ruined any and all good work done in the past for that patient. It's like a 10:1 ratio - 1 single bad moment can easily, 10 times, overshadow 10 good

moments in the patients memory. It's the same for all of us. We've had many a good experience (or "normal" experience we could say) visiting the doctor, but one (and for most there were not just one) bad experience overshadows the rest.

Like fast food too.....eat 100 burgers at a place just fine, but get one bad one and it's pretty hard to ever go back. I wish medical professionals would get this concept that they ethically, are there to serve the patient (within reason of course), and the patient isn't there just for them.

Subject: Re: depression and adverse cardiovascular eventsTo: hyperaldosteronism Date: Monday, July 25, 2011, 9:24 AM

The runaround that most of us have been given by the medical professionals, combined with the side effects of many of the drugs we have been prescribed, is in my opinion in and of itself enough to cause or exacerbate depression, anxiety, etc!> > > > > > > >> > > > > > > > Titre du document / Document title> > > > > > > > Increased plasma aldosterone in patients with clinical > > > > > depression> > >

> > > > > Auteur(s) / Author(s)> > > > > > > > EMANUELE Enzo ; GEROLDI Diego ; MINORETTI Piercarlo ; COEN > > > > > Enrico ; POLITI Pierluigi ;> > > > > > > > Résumé / Abstract> > > > > > > > Background. Clinical depression has been increasingly > > > > > recognized as an independent risk factor for adverse cardiovascular > > > > > events, but the biological mechanisms of this association remain > > > > > unclear. Recent evidence for reninsystem dysregulation in patients > > > > > with depression led us to hypothesize that aldosterone-a well- > > > > > recognized contributor to vascular injury-could be increased in > > > > > depressed patients. The present study was designed, therefore, to be > > > >

> a cross-sectional investigation of plasma renin and aldosterone > > > > > levels in depressed patients as compared with healthy controls with > > > > > no history of psychiatric illness. Methods. A total of 65 depressed > > > > > patients and 65 age- and gender-matched control subjects were > > > > > enrolled. Following a fixed sodium and potassium diet, venous blood > > > > > samples were obtained at 9:00 a.m. to avoid the influence of > > > > > circadian rhythms. Results. Although there were no significant > > > > > differences in plasma level of renin among subjects with depression > > > > > and controls (7.9 & #8242; 5.8 vs. 6.4 & #8242; 4.3 pg/mL, > > > > > respectively; p = 0.10), depressed subjects exhibited greater mean > > > > > aldosterone levels

as compared with control subjects (157.2 & #8242; > > > > > 67.5 vs. 125.7 & #8242; 38.1 pg/mL, respectively; p = 0.0014). After > > > > > adjusting for potential confounders, multivariate logistic > > > > > regression analysis showed that subjects with depression had 2.77 > > > > > times higher odds of elevated aldosterone levels compared with > > > > > healthy control subjects (95% confidence interval, 1.30-5.92, p = > > > > > 0.008). Conclusions. Our present findings support the hypothesis > > > > > that hyperaldosteronism could be a common feature among depressed > > > > > patients, thereby suggesting that increased aldosterone levels may > > > > > act as a mediator in the pathway linking depression to unfavorable > > > > > vascular events.> >

> > > > > > Revue / Journal Title> > > > > > > > Archives of medical research ISSN 0188-4409> > > > > > > > Source / Source> > > > > > > > 2005, vol. 36, no5, pp. 544-548 [5 page(s) (article)]> > > > > > > > Langue / Language> > > > > > > > Anglais> > > > > > > >> > > > > > > > Editeur / Publisher> > > > > > > > Elsevier, New York, NY, ETATS-UNIS (1992) (Revue)> > > > > > > >> > > > > > > > Localisation / Location> > > > > > > > INIST-CNRS, Cote INIST : 18673, 35400013278933.0200> > > > > > > >> > > > > > > >> > > > > > > > Nº notice refdoc (ud4) :

17228709> > > > > > > >> > > > > > >> > > > > > >> > > > > >> > > > >> > > > >> > > >> > >> >>

[Guest guest]

I have to remember that saying. Do you know who it is attrubuted to?

Subject: Re: depression and adverse cardiovascular eventsTo: hyperaldosteronism Date: Monday, July 25, 2011, 9:24 AM

The runaround that most of us have been given by the medical professionals, combined with the side effects of many of the drugs we have been prescribed, is in my opinion in and of itself enough to cause or exacerbate depression, anxiety, etc!> > > > > > > >> > > > > > > > Titre du document / Document title> > > > > > > > Increased plasma aldosterone in patients with clinical > > > > > depression> > > > > > > > Auteur(s) / Author(s)> > > > > > > > EMANUELE Enzo ; GEROLDI Diego ; MINORETTI Piercarlo ; COEN > > > >

> Enrico ; POLITI Pierluigi ;> > > > > > > > Résumé / Abstract> > > > > > > > Background. Clinical depression has been increasingly > > > > > recognized as an independent risk factor for adverse cardiovascular > > > > > events, but the biological mechanisms of this association remain > > > > > unclear. Recent evidence for reninsystem dysregulation in patients > > > > > with depression led us to hypothesize that aldosterone-a well- > > > > > recognized contributor to vascular injury-could be increased in > > > > > depressed patients. The present study was designed, therefore, to be > > > > > a cross-sectional investigation of plasma renin and aldosterone > > > > > levels in depressed patients as compared with healthy controls with >

> > > > no history of psychiatric illness. Methods. A total of 65 depressed > > > > > patients and 65 age- and gender-matched control subjects were > > > > > enrolled. Following a fixed sodium and potassium diet, venous blood > > > > > samples were obtained at 9:00 a.m. to avoid the influence of > > > > > circadian rhythms. Results. Although there were no significant > > > > > differences in plasma level of renin among subjects with depression > > > > > and controls (7.9 & #8242; 5.8 vs. 6.4 & #8242; 4.3 pg/mL, > > > > > respectively; p = 0.10), depressed subjects exhibited greater mean > > > > > aldosterone levels as compared with control subjects (157.2 & #8242; > > > > > 67.5 vs. 125.7 & #8242; 38.1 pg/mL, respectively; p = 0.0014). After > > >

> > adjusting for potential confounders, multivariate logistic > > > > > regression analysis showed that subjects with depression had 2.77 > > > > > times higher odds of elevated aldosterone levels compared with > > > > > healthy control subjects (95% confidence interval, 1.30-5.92, p = > > > > > 0.008). Conclusions. Our present findings support the hypothesis > > > > > that hyperaldosteronism could be a common feature among depressed > > > > > patients, thereby suggesting that increased aldosterone levels may > > > > > act as a mediator in the pathway linking depression to unfavorable > > > > > vascular events.> > > > > > > > Revue / Journal Title> > > > > > > > Archives of medical research ISSN 0188-4409> > > > > > >

> Source / Source> > > > > > > > 2005, vol. 36, no5, pp. 544-548 [5 page(s) (article)]> > > > > > > > Langue / Language> > > > > > > > Anglais> > > > > > > >> > > > > > > > Editeur / Publisher> > > > > > > > Elsevier, New York, NY, ETATS-UNIS (1992) (Revue)> > > > > > > >> > > > > > > > Localisation / Location> > > > > > > > INIST-CNRS, Cote INIST : 18673, 35400013278933.0200> > > > > > > >> > > > > > > >> > > > > > > > Nº notice refdoc (ud4) : 17228709> > > > > > > >> > > > > > >> > > > > > >> > > > > >> >

> > >> > > > >> > > >> > >> >>

[Guest guest]

AMEN msmith! When I was talking with my sister-in-law, a NP at DHMC, a few

years back she used the term " Clinical Depression " . I've included an article

from MayoClinic that describes it and you will find the DX process toward the

end (9 items) and you have to identify with atleast 5! I thought 8 out of 9

wasn't bad and add $50 per visit just for Phsyco Docs and $16/mo for Phsyco Meds

on top of the $56/mo for BP meds and 10's of $1000S for other Dr. Visits over

20+ years and all the symptoms associated with PA, YOU'RE DAMN RIGHT I'M

DEPRESSED! CERTIFIED!

But now that the mystery is over and now that I am in the " recovery phase " life

is a lot better and calmer! Thanks for convincing me to list the DX criteria

because I just reviewed it again and realize I am only at 1 out of 9 and I'm not

sure 8hrs a night with no naps is really sleeping too much!

- 64 yo morb. ob. male - 12mm X 13mm rt. a.adnoma with previous rt. flank &

testicle pain. I have decided against an adrenalectomy at this time since

Meds. are working so well. Current BP: 130/77

Other Issues/Opportunities: COPD w/ft Oxygen, OSA w Bi-Pap settings 13/19, DM2.

and PTSD

Meds: Duloxetine hcl 80 MG, Mirtazapine 15 MG, Metoprolol Tartrate 200 MG,

Metformin 2000MG and Spironolactone 75 MG.

MayoClinic.com reprints

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'Clinical depression': What does that mean?

By Mayo Clinic staff

--------------------------------------------------------------------------------

Original Article:http://www.mayoclinic.com/health/clinical-depression/AN01057

--------------------------------------------------------------------------------

With Mayo Clinic psychiatrist K. Hall-Flavin, M.D.read biography close

window Biography of K. Hall-Flavin, M.D. K. Hall-Flavin, M.D.

--------------------------------------------------------------------------------

Dr. Hall-Flavin, board certified in general psychiatry and addiction

psychiatry, is a St. Louis native looking to the Internet as a way to help

people improve their health and be more active participants in their own health

care by learning from Mayo Clinic's experts.

Dr. Hall-Flavin served on the faculties of Cornell University Medical College,

New York Medical College and The Washington University Medical School

before joining the Mayo Clinic staff in 1996. He has special interests in adult

psychiatry, addiction psychiatry, pharmacogenetics and personalized medicine. He

served as medical director of the National Council on Alcoholism and Drug

Dependence from 1986 to 1999, and is currently involved in translational

medicine research involving the introduction of pharmacogenetic technology into

the daily practice of community psychiatry.

" With the advent of pharmacogenetics and related fields and the advances in

translational medicine, informed collaborative relationships between

knowledgeable, capable health professionals and informed, proactive individuals

and their families are more vital than ever, " he said.

" I'm optimistic that our Internet health education activities will contribute to

ever-improving health outcomes for all who participate and apply what is

learned. "

Definition (1)'Clinical depression': What does that mean?Risk factors (1)Junk

food blues: Are depression and diet related?Symptoms (2)Nervous breakdown: What

does it mean?Pain and depression: Is there a link?Causes (4)Vitamin B-12 and

depression: Are they related?Caffeine and depression: Is there a link?Marijuana

and depression: What's the link?see all in CausesComplications (2)Depression and

anxiety: Can I have both?Tinnitus causes: Could my antidepressant be the

culprit?Treatments and drugs (8)Mild depression: Are antidepressants

effective?Antidepressants: Can they stop working?Antidepressants and alcohol:

What is the concern?see all in Treatments and drugsAlternative medicine (2)Fish

oil supplements: Can they treat depression?Natural remedies for depression: Are

they effective?Connect with others who've been there. Share stories. Learn. Join

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Question

'Clinical depression': What does that mean?

What does the term " clinical depression " mean?

Answer

from K. Hall-Flavin, M.D.

Depression ranges in seriousness from mild, temporary episodes of sadness to

severe, persistent depression. Doctors use the term " clinical depression " to

describe the more severe form of depression also known as " major depression " or

" major depressive disorder. "

For a diagnosis of clinical depression, you must meet the symptom criteria

spelled out in the Diagnostic and Statistical Manual of Mental Disorders (DSM).

The DSM is a guidebook used to diagnose mental illness in the United States.

Clinical depression symptoms may include:

•Depressed mood most of the day, nearly every day

•Loss of interest or pleasure in most activities

•Significant weight loss or gain

•Sleeping too much or not being able to sleep nearly every day

•Slowed thinking or movement that others can see

•Fatigue or low energy nearly every day

•Feelings of worthlessness or inappropriate guilt

•Loss of concentration or indecisiveness

•Recurring thoughts of death or suicide

To meet the criteria for clinical depression (called major depression in the

DSM), you must have five or more of the above symptoms over a two-week period.

At least one of the symptoms must be either a depressed mood or a loss of

interest or pleasure. Keep in mind, some types of depression may not fit this

strict definition.

Clinical depression causes noticeable disruptions in daily life, such as work,

school or social activities. It can affect people of any age or sex, including

children. It isn't the same as depression caused by a loss (such as the death of

a loved one), substance abuse or a medical condition such as a thyroid disorder.

Clinical depression symptoms usually improve with psychological counseling,

antidepressant medications or a combination of the two. Even severe depression

symptoms usually improve with treatment.

Next questionJunk food blues: Are depression and diet related?

See AlsoHand Scheduled

Section Focus Welcome to our new depression blogIt's a SAD time of yearMental

health: What's normal, what's notPostpartum depression

[Guest guest]

I got it from dr Eugene A Stead, Duke, the founder of PA concept and program. There is a web site called "just say for me" that has many of his quotes. Tiped sad Send form miiPhone ;-)May your pressure be low!CE Grim MDSpecializing in DifficultHypertension

I have to remember that saying. Do you know who it is attrubuted to?

Subject: Re: depression and adverse cardiovascular eventsTo: hyperaldosteronism Date: Monday, July 25, 2011, 9:24 AM

The runaround that most of us have been given by the medical professionals, combined with the side effects of many of the drugs we have been prescribed, is in my opinion in and of itself enough to cause or exacerbate depression, anxiety, etc!> > > > > > > >> > > > > > > > Titre du document / Document title> > > > > > > > Increased plasma aldosterone in patients with clinical > > > > > depression> > > > > > > > Auteur(s) / Author(s)> > > > > > > > EMANUELE Enzo ; GEROLDI Diego ; MINORETTI Piercarlo ; COEN > > > >

> Enrico ; POLITI Pierluigi ;> > > > > > > > Résumé / Abstract> > > > > > > > Background. Clinical depression has been increasingly > > > > > recognized as an independent risk factor for adverse cardiovascular > > > > > events, but the biological mechanisms of this association remain > > > > > unclear. Recent evidence for reninsystem dysregulation in patients > > > > > with depression led us to hypothesize that aldosterone-a well- > > > > > recognized contributor to vascular injury-could be increased in > > > > > depressed patients. The present study was designed, therefore, to be > > > > > a cross-sectional investigation of plasma renin and aldosterone > > > > > levels in depressed patients as compared with healthy controls with >

> > > > no history of psychiatric illness. Methods. A total of 65 depressed > > > > > patients and 65 age- and gender-matched control subjects were > > > > > enrolled. Following a fixed sodium and potassium diet, venous blood > > > > > samples were obtained at 9:00 a.m. to avoid the influence of > > > > > circadian rhythms. Results. Although there were no significant > > > > > differences in plasma level of renin among subjects with depression > > > > > and controls (7

[Guest guest]

From: " Eugene A. Stead Jr. A life of chasing what I did not understand "

Contributor: Clarence Grim

Title: Another Kempner Story

The service had a 70 year old woman with severe aortic insufficiency who

developed (again) flagrant congestive heart failure after eating at a pizza

place. The only thing she was being treated with was distilled water to drink

and the Kempner colored pill, which were placebos. Amazingly (to me) her heart

size quickly decreased to nearly normal and her signs and symptoms of CHF

disappeared.

I told Dr. K that I thought she needed to have her aortic valve replaced.

" Dr. Grim, " he said, " I have been taking care of this lady for a number of

years. As long as she stays away from salt she does not have heart failure. Two

of the last four patients I have sent for aortic valve replacement have died

soon after surgery. I think she is safer avoiding salt. "

I suspect this and other patients seen on Dr. K's service as well as Dr. Stead's

statements a number of times during my 3 years, " Dr. Kempner is the smartest

doctor at Duke Hospital! " forged my interest in the role of salt and blood

pressure that has driven my career for almost 40 years. I still use slides from

Dr. K's papers every time I talk about high blood pressure.

I guess that sums it up! (It's the Salt and operate only if Meds. and DASH

don't work!) Great site Dr. G., I've bookmarked it!

- 64 yo morb. ob. male - 12mm X 13mm rt. a.adnoma with previous rt. flank &

testicle pain. I have decided against an adrenalectomy at this time since

Meds. are working so well. Current BP: 130/77

Other Issues/Opportunities: COPD w/ft Oxygen, OSA w Bi-Pap settings 13/19, DM2.

and PTSD

Meds: Duloxetine hcl 80 MG, Mirtazapine 15 MG, Metoprolol Tartrate 200 MG,

Metformin 2000MG and Spironolactone 75 MG.

> >> > > > > > > > >

> >> > > > > > > > > Titre du document / Document title

> >> > > > > > > > > Increased plasma aldosterone in patients with clinical

> >> > > > > > depression

> >> > > > > > > > > Auteur(s) / Author(s)

> >> > > > > > > > > EMANUELE Enzo ; GEROLDI Diego ; MINORETTI Piercarlo ; COEN

> >> > > > > > Enrico ; POLITI Pierluigi ;

> >> > > > > > > > > Résumé / Abstract

> >> > > > > > > > > Background. Clinical depression has been increasingly

> >> > > > > > recognized as an independent risk factor for adverse

cardiovascular

> >> > > > > > events, but the biological mechanisms of this association remain

> >> > > > > > unclear. Recent evidence for reninsystem dysregulation in

patients

> >> > > > > > with depression led us to hypothesize that aldosterone-a well-

> >> > > > > > recognized contributor to vascular injury-could be increased in

> >> > > > > > depressed patients. The present study was designed, therefore, to

be

> >> > > > > > a cross-sectional investigation of plasma renin and aldosterone

> >> > > > > > levels in depressed patients as compared with healthy controls

with

> >> > > > > > no history of psychiatric illness. Methods. A total of 65

depressed

> >> > > > > > patients and 65 age- and gender-matched control subjects were

> >> > > > > > enrolled. Following a fixed sodium and potassium diet, venous

blood

> >> > > > > > samples were obtained at 9:00 a.m. to avoid the influence of

> >> > > > > > circadian rhythms. Results. Although there were no significant

> >> > > > > > differences in plasma level of renin among subjects with

depression

> >> > > > > > and controls (7

>

[Guest guest]

BTW my bias is that all diseases are organic.CE Grim MD I prefer the term "emotional health" problems as "mental health" seems to imply an organic disorder that is permanent. And sometimes it is "iatrogenic" - physician (or any medical professional) caused. I used to lecture on this when I was on the faculty in Oklahoma at State University in terms of paramedics, wherein medics are viewed as "lifesavers" by the general public, when in truth rarely did we truly save a life, but we impacted every life we came in contact with every day - so even for mere minutes with a patient it only took ONE single incident of rudeness, overt arrogance, or some negative moment and THAT is what the patient remembered forever and that one moment ruined any and all good work done in the past for that patient. It's like a 10:1 ratio - 1 single bad moment can easily, 10 times, overshadow 10 good moments in the patients memory. It's the same for all of us. We've had many a good experience (or "normal" experience we could say) visiting the doctor, but one (and for most there were not just one) bad experience overshadows the rest. Like fast food too.....eat 100 burgers at a place just fine, but get one bad one and it's pretty hard to ever go back. I wish medical professionals would get this concept that they ethically, are there to serve the patient (within reason of course), and the patient isn't there just for them. Subject: Re: depression and adverse cardiovascular eventsTo: hyperaldosteronism Date: Monday, July 25, 2011, 9:24 AM The runaround that most of us have been given by the medical professionals, combined with the side effects of many of the drugs we have been prescribed, is in my opinion in and of itself enough to cause or exacerbate depression, anxiety, etc!> > > > > > > >> > > > > > > > Titre du document / Document title> > > > > > > > Increased plasma aldosterone in patients with clinical > > > > > depression> > > > > > > > Auteur(s) / Author(s)> > > > > > > > EMANUELE Enzo ; GEROLDI Diego ; MINORETTI Piercarlo ; COEN > > > > > Enrico ; POLITI Pierluigi ;> > > > > > > > Résumé / Abstract> > > > > > > > Background. Clinical depression has been increasingly > > > > > recognized as an independent risk factor for adverse cardiovascular > > > > > events, but the biological mechanisms of this association remain > > > > > unclear. Recent evidence for reninsystem dysregulation in patients > > > > > with depression led us to hypothesize that aldosterone-a well- > > > > > recognized contributor to vascular injury-could be increased in > > > > > depressed patients. The present study was designed, therefore, to be > > > > > a cross-sectional investigation of plasma renin and aldosterone > > > > > levels in depressed patients as compared with healthy controls with > > > > > no history of psychiatric illness. Methods. A total of 65 depressed > > > > > patients and 65 age- and gender-matched control subjects were > > > > > enrolled. Following a fixed sodium and potassium diet, venous blood > > > > > samples were obtained at 9:00 a.m. to avoid the influence of > > > > > circadian rhythms. Results. Although there were no significant > > > > > differences in plasma level of renin among subjects with depression > > > > > and controls (7.9 & #8242; 5.8 vs. 6.4 & #8242; 4.3 pg/mL, > > > > > respectively; p = 0.10), depressed subjects exhibited greater mean > > > > > aldosterone levels as compared with control subjects (157.2 & #8242; > > > > > 67.5 vs. 125.7 & #8242; 38.1 pg/mL, respectively; p = 0.0014). After > > > > > adjusting for potential confounders, multivariate logistic > > > > > regression analysis showed that subjects with depression had 2.77 > > > > > times higher odds of elevated aldosterone levels compared with > > > > > healthy control subjects (95% confidence interval, 1.30-5.92, p = > > > > > 0.008). Conclusions. Our present findings support the hypothesis > > > > > that hyperaldosteronism could be a common feature among depressed > > > > > patients, thereby suggesting that increased aldosterone levels may > > > > > act as a mediator in the pathway linking depression to unfavorable > > > > > vascular events.> > > > > > > > Revue / Journal Title> > > > > > > > Archives of medical research ISSN 0188-4409> > > > > > > > Source / Source> > > > > > > > 2005, vol. 36, no5, pp. 544-548 [5 page(s) (article)]> > > > > > > > Langue / Language> > > > > > > > Anglais> > > > > > > >> > > > > > > > Editeur / Publisher> > > > > > > > Elsevier, New York, NY, ETATS-UNIS (1992) (Revue)> > > > > > > >> > > > > > > > Localisation / Location> > > > > > > > INIST-CNRS, Cote INIST : 18673, 35400013278933.0200> > > > > > > >> > > > > > > >> > > > > > > > Nº notice refdoc (ud4) : 17228709> > > > > > > >> > > > > > >> > > > > > >> > > > > >> > > > >> > > > >> > > >> > >> >>

[Guest guest]

Many that have mental health problems have something that is permanent.

Treatment is somewhat limited and as of yet there is no cure.

Many in my family have mental health problems.

> > > > > > > > >

> > > > > > > > > Titre du document / Document title

> > > > > > > > > Increased plasma aldosterone in patients with clinical

> > > > > > depression

> > > > > > > > > Auteur(s) / Author(s)

> > > > > > > > > EMANUELE Enzo ; GEROLDI Diego ; MINORETTI Piercarlo ; COEN

> > > > > > Enrico ; POLITI Pierluigi ;

> > > > > > > > > Résumé / Abstract

> > > > > > > > > Background. Clinical depression has been increasingly

> > > > > > recognized as an independent risk factor for adverse cardiovascular

> > > > > > events, but the biological mechanisms of this association remain

> > > > > > unclear. Recent evidence for reninsystem dysregulation in patients

> > > > > > with depression led us to hypothesize that aldosterone-a well-

> > > > > > recognized contributor to vascular injury-could be increased in

> > > > > > depressed patients. The present study was designed, therefore, to be

> > > > > > a cross-sectional investigation of plasma renin and aldosterone

> > > > > > levels in depressed patients as compared with healthy controls with

> > > > > > no history of psychiatric illness. Methods. A total of 65 depressed

> > > > > > patients and 65 age- and gender-matched control subjects were

> > > > > > enrolled. Following a fixed sodium and potassium diet, venous blood

> > > > > > samples were obtained at 9:00 a.m. to avoid the influence of

> > > > > > circadian rhythms. Results. Although there were no significant

> > > > > > differences in plasma level of renin among subjects with depression

> > > > > > and controls (7.9 & #8242; 5.8 vs. 6.4 & #8242; 4.3 pg/mL,

> > > > > > respectively; p = 0.10), depressed subjects exhibited greater mean

> > > > > > aldosterone levels as compared with control subjects (157.2 & #8242;

> > > > > > 67.5 vs. 125.7 & #8242; 38.1 pg/mL, respectively; p = 0.0014). After

> > > > > > adjusting for potential confounders, multivariate logistic

> > > > > > regression analysis showed that subjects with depression had 2.77

> > > > > > times higher odds of elevated aldosterone levels compared with

> > > > > > healthy control subjects (95% confidence interval, 1.30-5.92, p =

> > > > > > 0.008). Conclusions. Our present findings support the hypothesis

> > > > > > that hyperaldosteronism could be a common feature among depressed

> > > > > > patients, thereby suggesting that increased aldosterone levels may

> > > > > > act as a mediator in the pathway linking depression to unfavorable

> > > > > > vascular events.

> > > > > > > > > Revue / Journal Title

> > > > > > > > > Archives of medical research ISSN 0188-4409

> > > > > > > > > Source / Source

> > > > > > > > > 2005, vol. 36, no5, pp. 544-548 [5 page(s) (article)]

> > > > > > > > > Langue / Language

> > > > > > > > > Anglais

> > > > > > > > >

> > > > > > > > > Editeur / Publisher

> > > > > > > > > Elsevier, New York, NY, ETATS-UNIS (1992) (Revue)

> > > > > > > > >

> > > > > > > > > Localisation / Location

> > > > > > > > > INIST-CNRS, Cote INIST : 18673, 35400013278933.0200

> > > > > > > > >

> > > > > > > > >

> > > > > > > > > Nº notice refdoc (ud4) : 17228709

> > > > > > > > >

> > > > > > > >

> > > > > > > >

> > > > > > >

> > > > > >

> > > > > >

> > > > >

> > > >

> > >

> >

>

[Guest guest]

But the original idea in this post was if PA caused it or not - if so then then the anxiety or depression is not a permanent issue - but a temporary one - and then is it a real "mental health" issue or is it a physical issue leading to the other problem. If one already has those issues then PA could only exacerbate them. Then we would have to ask is that because that person responds to bad news or illness with depression and/or anxiety anyway, which would mean ANY illness may have done that to someone prone to those emotions.

It would be natural for many people when told they have PA and had suffered with symptoms for a long time to maybe get down or anxious about the unknown. That would surely be in the realm of an expected response and doesn't mean someone suffers from depression or anxiety. We have become a society where somehow the message got out that NO ONE should EVER feel a negative emotion and people run to get "something" when someone dies, or they get laid off, or have a relationship issue and of course they are lucky enough to get diagnosed as "depression" or "anxiety disorder" or "bipolar" because their mood is not puppies ad rainbows every day. The serious issue is once they do get labeled then ANY emotion that is not upbeat and positive is seen as bad and they think they should never ever feel any sad or mad or worried emotion. And many of us have a tendency when we feel something not so good, to blame it on the other thing in our life, like PA. Maybe it

is, maybe it aint.

Subject: Re: depression and adverse cardiovascular eventsTo: hyperaldosteronism Date: Monday, July 25, 2011, 7:36 PM

Many that have mental health problems have something that is permanent. Treatment is somewhat limited and as of yet there is no cure. Many in my family have mental health problems. > > > > > > > > >> > > > > > > > > Titre du document / Document title> > > > > > > > > Increased plasma aldosterone in patients with clinical > > >

> > > depression> > > > > > > > > Auteur(s) / Author(s)> > > > > > > > > EMANUELE Enzo ; GEROLDI Diego ; MINORETTI Piercarlo ; COEN > > > > > > Enrico ; POLITI Pierluigi ;> > > > > > > > > Résumé / Abstract> > > > > > > > > Background. Clinical depression has been increasingly > > > > > > recognized as an independent risk factor for adverse cardiovascular > > > > > > events, but the biological mechanisms of this association remain > > > > > > unclear. Recent evidence for reninsystem dysregulation in patients > > > > > > with depression led us to hypothesize that aldosterone-a well- > > > > > > recognized contributor to vascular injury-could be increased in > > > >

> > depressed patients. The present study was designed, therefore, to be > > > > > > a cross-sectional investigation of plasma renin and aldosterone > > > > > > levels in depressed patients as compared with healthy controls with > > > > > > no history of psychiatric illness. Methods. A total of 65 depressed > > > > > > patients and 65 age- and gender-matched control subjects were > > > > > > enrolled. Following a fixed sodium and potassium diet, venous blood > > > > > > samples were obtained at 9:00 a.m. to avoid the influence of > > > > > > circadian rhythms. Results. Although there were no significant > > > > > > differences in plasma level of renin among subjects with depression > > > > > > and controls (7.9 & #8242; 5.8 vs. 6.4 & #8242; 4.3

pg/mL, > > > > > > respectively; p = 0.10), depressed subjects exhibited greater mean > > > > > > aldosterone levels as compared with control subjects (157.2 & #8242; > > > > > > 67.5 vs. 125.7 & #8242; 38.1 pg/mL, respectively; p = 0.0014). After > > > > > > adjusting for potential confounders, multivariate logistic > > > > > > regression analysis showed that subjects with depression had 2.77 > > > > > > times higher odds of elevated aldosterone levels compared with > > > > > > healthy control subjects (95% confidence interval, 1.30-5.92, p = > > > > > > 0.008). Conclusions. Our present findings support the hypothesis > > > > > > that hyperaldosteronism could be a common feature among depressed > > > > > > patients, thereby

suggesting that increased aldosterone levels may > > > > > > act as a mediator in the pathway linking depression to unfavorable > > > > > > vascular events.> > > > > > > > > Revue / Journal Title> > > > > > > > > Archives of medical research ISSN 0188-4409> > > > > > > > > Source / Source> > > > > > > > > 2005, vol. 36, no5, pp. 544-548 [5 page(s) (article)]> > > > > > > > > Langue / Language> > > > > > > > > Anglais> > > > > > > > >> > > > > > > > > Editeur / Publisher> > > > > > > > > Elsevier, New York, NY, ETATS-UNIS (1992) (Revue)> > > > > > > > >> > > > > > > > >

Localisation / Location> > > > > > > > > INIST-CNRS, Cote INIST : 18673, 35400013278933.0200> > > > > > > > >> > > > > > > > >> > > > > > > > > Nº notice refdoc (ud4) : 17228709> > > > > > > > >> > > > > > > >> > > > > > > >> > > > > > >> > > > > >> > > > > >> > > > >> > > >> > >> >>

[Guest guest]

If high aldo is the cause of anxiety or depression

does cutting back on salt have the same affect on the anxiety or depression as

it does on lowing B/P?

> > > > > > > > > >

> > > > > > > > > > Titre du document / Document title

> > > > > > > > > > Increased plasma aldosterone in patients with clinical

> > > > > > > depression

> > > > > > > > > > Auteur(s) / Author(s)

> > > > > > > > > > EMANUELE Enzo ; GEROLDI Diego ; MINORETTI Piercarlo ; COEN

> > > > > > > Enrico ; POLITI Pierluigi ;

> > > > > > > > > > RÃÆ'©sumÃÆ'© / Abstract

> > > > > > > > > > Background. Clinical depression has been increasingly

> > > > > > > recognized as an independent risk factor for adverse

cardiovascular

> > > > > > > events, but the biological mechanisms of this association remain

> > > > > > > unclear. Recent evidence for reninsystem dysregulation in patients

> > > > > > > with depression led us to hypothesize that aldosterone-a well-

> > > > > > > recognized contributor to vascular injury-could be increased in

> > > > > > > depressed patients. The present study was designed, therefore, to

be

> > > > > > > a cross-sectional investigation of plasma renin and aldosterone

> > > > > > > levels in depressed patients as compared with healthy controls

with

> > > > > > > no history of psychiatric illness. Methods. A total of 65

depressed

> > > > > > > patients and 65 age- and gender-matched control subjects were

> > > > > > > enrolled. Following a fixed sodium and potassium diet, venous

blood

> > > > > > > samples were obtained at 9:00 a.m. to avoid the influence of

> > > > > > > circadian rhythms. Results. Although there were no significant

> > > > > > > differences in plasma level of renin among subjects with

depression

> > > > > > > and controls (7.9 & #8242; 5.8 vs. 6.4 & #8242; 4.3 pg/mL,

> > > > > > > respectively; p = 0.10), depressed subjects exhibited greater mean

> > > > > > > aldosterone levels as compared with control subjects (157.2

& #8242;

> > > > > > > 67.5 vs. 125.7 & #8242; 38.1 pg/mL, respectively; p = 0.0014).

After

> > > > > > > adjusting for potential confounders, multivariate logistic

> > > > > > > regression analysis showed that subjects with depression had 2.77

> > > > > > > times higher odds of elevated aldosterone levels compared with

> > > > > > > healthy control subjects (95% confidence interval, 1.30-5.92, p =

> > > > > > > 0.008). Conclusions. Our present findings support the hypothesis

> > > > > > > that hyperaldosteronism could be a common feature among depressed

> > > > > > > patients, thereby suggesting that increased aldosterone levels may

> > > > > > > act as a mediator in the pathway linking depression to unfavorable

> > > > > > > vascular events.

> > > > > > > > > > Revue / Journal Title

> > > > > > > > > > Archives of medical research ISSN 0188-4409

> > > > > > > > > > Source / Source

> > > > > > > > > > 2005, vol. 36, no5, pp. 544-548 [5 page(s) (article)]

> > > > > > > > > > Langue / Language

> > > > > > > > > > Anglais

> > > > > > > > > >

> > > > > > > > > > Editeur / Publisher

> > > > > > > > > > Elsevier, New York, NY, ETATS-UNIS (1992) (Revue)

> > > > > > > > > >

> > > > > > > > > > Localisation / Location

> > > > > > > > > > INIST-CNRS, Cote INIST : 18673, 35400013278933.0200

> > > > > > > > > >

> > > > > > > > > >

> > > > > > > > > > Nº notice refdoc (ud4) : 17228709

> > > > > > > > > >

> > > > > > > > >

> > > > > > > > >

> > > > > > > >

> > > > > > >

> > > > > > >

> > > > > >

> > > > >

> > > >

> > >

> >

>

[Guest guest]

Most bad effects of aldo seem to require a high salt intake so the same should be true for aldo and depression. But not one that has been tested properly.CE Grim MDOn Jul 26, 2011, at 8:17 PM, Francis Bill SUSPECTED PA wrote: If high aldo is the cause of anxiety or depression does cutting back on salt have the same affect on the anxiety or depression as it does on lowing B/P? > > > > > > > > > > > > > > > > > > > > Titre du document / Document title > > > > > > > > > > Increased plasma aldosterone in patients with clinical > > > > > > > depression > > > > > > > > > > Auteur(s) / Author(s) > > > > > > > > > > EMANUELE Enzo ; GEROLDI Diego ; MINORETTI Piercarlo ; COEN > > > > > > > Enrico ; POLITI Pierluigi ; > > > > > > > > > > RÃÆ'©sumÃÆ'© / Abstract > > > > > > > > > > Background. Clinical depression has been increasingly > > > > > > > recognized as an independent risk factor for adverse cardiovascular > > > > > > > events, but the biological mechanisms of this association remain > > > > > > > unclear. Recent evidence for reninsystem dysregulation in patients > > > > > > > with depression led us to hypothesize that aldosterone-a well- > > > > > > > recognized contributor to vascular injury-could be increased in > > > > > > > depressed patients. The present study was designed, therefore, to be > > > > > > > a cross-sectional investigation of plasma renin and aldosterone > > > > > > > levels in depressed patients as compared with healthy controls with > > > > > > > no history of psychiatric illness. Methods. A total of 65 depressed > > > > > > > patients and 65 age- and gender-matched control subjects were > > > > > > > enrolled. Following a fixed sodium and potassium diet, venous blood > > > > > > > samples were obtained at 9:00 a.m. to avoid the influence of > > > > > > > circadian rhythms. Results. Although there were no significant > > > > > > > differences in plasma level of renin among subjects with depression > > > > > > > and controls (7.9 & #8242; 5.8 vs. 6.4 & #8242; 4.3 pg/mL, > > > > > > > respectively; p = 0.10), depressed subjects exhibited greater mean > > > > > > > aldosterone levels as compared with control subjects (157.2 & #8242; > > > > > > > 67.5 vs. 125.7 & #8242; 38.1 pg/mL, respectively; p = 0.0014). After > > > > > > > adjusting for potential confounders, multivariate logistic > > > > > > > regression analysis showed that subjects with depression had 2.77 > > > > > > > times higher odds of elevated aldosterone levels compared with > > > > > > > healthy control subjects (95% confidence interval, 1.30-5.92, p = > > > > > > > 0.008). Conclusions. Our present findings support the hypothesis > > > > > > > that hyperaldosteronism could be a common feature among depressed > > > > > > > patients, thereby suggesting that increased aldosterone levels may > > > > > > > act as a mediator in the pathway linking depression to unfavorable > > > > > > > vascular events. > > > > > > > > > > Revue / Journal Title > > > > > > > > > > Archives of medical research ISSN 0188-4409 > > > > > > > > > > Source / Source > > > > > > > > > > 2005, vol. 36, no5, pp. 544-548 [5 page(s) (article)] > > > > > > > > > > Langue / Language > > > > > > > > > > Anglais > > > > > > > > > > > > > > > > > > > > Editeur / Publisher > > > > > > > > > > Elsevier, New York, NY, ETATS-UNIS (1992) (Revue) > > > > > > > > > > > > > > > > > > > > Localisation / Location > > > > > > > > > > INIST-CNRS, Cote INIST : 18673, 35400013278933.0200 > > > > > > > > > > > > > > > > > > > > > > > > > > > > > > Nº notice refdoc (ud4) : 17228709 > > > > > > > > > > > > > > > > > > > > > > > > > > > > > > > > > > > > > > > > > > > > > > > > > > > > > > > > > > > > > > > > > > > > > > >

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Could be.CE grim MDOn Jul 26, 2011, at 9:50 PM, Francis Bill SUSPECTED PA wrote: Most are also taking Sprio. could be it is the sprio treating the anxiety or depression. > > > > > > > > > > > > > > > > > > > > > > > > Titre du document / Document title > > > > > > > > > > > > Increased plasma aldosterone in patients with > > clinical > > > > > > > > > depression > > > > > > > > > > > > Auteur(s) / Author(s) > > > > > > > > > > > > EMANUELE Enzo ; GEROLDI Diego ; MINORETTI > > Piercarlo ; COEN > > > > > > > > > Enrico ; POLITI Pierluigi ; > > > > > > > > > > > > RÃÆ'©sumÃÆ'© / Abstract > > > > > > > > > > > > Background. Clinical depression has been > > increasingly > > > > > > > > > recognized as an independent risk factor for adverse > > cardiovascular > > > > > > > > > events, but the biological mechanisms of this > > association remain > > > > > > > > > unclear. Recent evidence for reninsystem dysregulation > > in patients > > > > > > > > > with depression led us to hypothesize that aldosterone- > > a well- > > > > > > > > > recognized contributor to vascular injury-could be > > increased in > > > > > > > > > depressed patients. The present study was designed, > > therefore, to be > > > > > > > > > a cross-sectional investigation of plasma renin and > > aldosterone > > > > > > > > > levels in depressed patients as compared with healthy > > controls with > > > > > > > > > no history of psychiatric illness. Methods. A total of > > 65 depressed > > > > > > > > > patients and 65 age- and gender-matched control > > subjects were > > > > > > > > > enrolled. Following a fixed sodium and potassium diet, > > venous blood > > > > > > > > > samples were obtained at 9:00 a.m. to avoid the > > influence of > > > > > > > > > circadian rhythms. Results. Although there were no > > significant > > > > > > > > > differences in plasma level of renin among subjects > > with depression > > > > > > > > > and controls (7.9 & #8242; 5.8 vs. 6.4 & #8242; 4.3 pg/mL, > > > > > > > > > respectively; p = 0.10), depressed subjects exhibited > > greater mean > > > > > > > > > aldosterone levels as compared with control subjects > > (157.2 & #8242; > > > > > > > > > 67.5 vs. 125.7 & #8242; 38.1 pg/mL, respectively; p = > > 0.0014). After > > > > > > > > > adjusting for potential confounders, multivariate > > logistic > > > > > > > > > regression analysis showed that subjects with > > depression had 2.77 > > > > > > > > > times higher odds of elevated aldosterone levels > > compared with > > > > > > > > > healthy control subjects (95% confidence interval, > > 1.30-5.92, p = > > > > > > > > > 0.008). Conclusions. Our present findings support the > > hypothesis > > > > > > > > > that hyperaldosteronism could be a common feature > > among depressed > > > > > > > > > patients, thereby suggesting that increased > > aldosterone levels may > > > > > > > > > act as a mediator in the pathway linking depression to > > unfavorable > > > > > > > > > vascular events. > > > > > > > > > > > > Revue / Journal Title > > > > > > > > > > > > Archives of medical research ISSN 0188-4409 > > > > > > > > > > > > Source / Source > > > > > > > > > > > > 2005, vol. 36, no5, pp. 544-548 [5 page(s) > > (article)] > > > > > > > > > > > > Langue / Language > > > > > > > > > > > > Anglais > > > > > > > > > > > > > > > > > > > > > > > > Editeur / Publisher > > > > > > > > > > > > Elsevier, New York, NY, ETATS-UNIS (1992) (Revue) > > > > > > > > > > > > > > > > > > > > > > > > Localisation / Location > > > > > > > > > > > > INIST-CNRS, Cote INIST : 18673, > > 35400013278933.0200 > > > > > > > > > > > > > > > > > > > > > > > > > > > > > > > > > > > > Nº notice refdoc (ud4) : 17228709 > > > > > > > > > > > > > > > > > > > > > > > > > > > > > > > > > > > > > > > > > > > > > > > > > > > > > > > > > > > > > > > > > > > > > > > > > > > > > > > > > > > > > > > > > > > > > > > > > > > >