PA only a problem with increased salt intake?

[Guest guest]

Dr Grim,

Just to be clear, even if you have PA it is only a problem with

increased sodium intake?

Phyllis

[Guest guest]

Just to be clear- a necessary and sufficient condition for ALDO to do its damage is a high salt diet. A low K diet will worsen the effects of excess Na. This is the reason I have pushed the DASH and many report such good improvement in Sx and BP. May your pressure be low!CE Grim MS, MDSpecializing in DifficultHypertensionOn May 22, 2012, at 20:28, Phyllis <phylisrn@...> wrote:

Dr Grim,

Just to be clear, even if you have PA it is only a problem with

increased sodium intake?

Phyllis

[Guest guest]

High Aldo may also cause depression

http://www.ncbi.nlm.nih.gov/pubmed/21375792

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 ìg/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.

PMID:21375792[PubMed - in process]

>

> > Dr Grim,

> > Just to be clear, even if you have PA it is only a problem with

> > increased sodium intake?

> >

> > Phyllis

> >

>

[Guest guest]

High Aldo may also cause depression

http://www.ncbi.nlm.nih.gov/pubmed/21375792

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 ìg/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.

PMID:21375792[PubMed - in process]

>

> > Dr Grim,

> > Just to be clear, even if you have PA it is only a problem with

> > increased sodium intake?

> >

> > Phyllis

> >

>

[Guest guest]

If you do a search for aldosterone and depression will find more information on

it.

> >

> > > Dr Grim,

> > > Just to be clear, even if you have PA it is only a problem with

> > > increased sodium intake?

> > >

> > > Phyllis

> > >

> >

>

[Guest guest]

If you do a search for aldosterone and depression will find more information on

it.

> >

> > > Dr Grim,

> > > Just to be clear, even if you have PA it is only a problem with

> > > increased sodium intake?

> > >

> > > Phyllis

> > >

> >

>

[Guest guest]

Interesting study. At least if you have a white fur coat.CE Grim MDOn May 23, 2012, at 6:34 AM, Francis Bill SUSPECTED PA wrote: High Aldo may also cause depression http://www.ncbi.nlm.nih.gov/pubmed/21375792 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 ìg/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. PMID:21375792[PubMed - in process] > > > Dr Grim, > > Just to be clear, even if you have PA it is only a problem with > > increased sodium intake? > > > > Phyllis > > >

[Guest guest]

On 5/22/2012 9:28 PM, Phyllis wrote:

> Dr Grim,

> Just to be clear, even if you have PA it is only a problem with

> increased sodium intake?

>

> Phyllis

Good Article:

Effects of Exercise, Diet and Weight

Loss on High Blood Pressure

http://www.portalsaudebrasil.com/artigospsb/obes064.pdf

[Guest guest]

It's not an "increased" salt intake for the normal person. The latest recommendations, I believe from memory for healthy living, are keeping it below 2300mg a day. Recommendations in PA and DASH are 1500 per day. So what the person without PA can have, we can't. So a "normal" salt intake is the problem. An "increased" intake might be a killer for us.

I can only speak from my experience this last year or two, and 1500 is about right on for me (I didn't get real serious about DASH until early 2011). Get over that amount , and sure as you know what my BP rises, If I keep it below that - and keep the soda intake way down, and exercise, I don't have to take the spiro - which does hurt my boobies after a bit. And I am well spoken about how high and uncontrollable I was before PA was discovered by testing it with the spiro and 170/130 on any day was nothing for me. I am only grateful I was a healthy and in shape man when PA (HTN and low K symptoms) reared it's head around 2003/2004 because I was that high for years even on as many as 5 meds at once.

I will just add again, for those reading or new to this that I am not fanatical about anything. But I have been able to cut out and down my meds with DASH and controlling my K so I have energy to exercise. DASH for me meant mostly cutting out packaged stuff and fast food - and soda (I love my pepsi and still drink it, but not often now), and just changing some habits. Now, I know people are different, my wife is more OCD and I am surely ADD and she would be fanatical if she stuck to DASH but for me I have had to be tricky and just learn to cut this or that out - make sure I have more raw veggies and fruits for snacks (I know some can't eat the same foods, but find what works for you) and I enjoy things I always have, just more moderate. And it works and I keep mine under 1500 sodium a day. > Dr Grim,> Just to be clear, even if you have PA it is only a problem with > increased sodium intake?>> PhyllisGood Article:Effects of Exercise, Diet and WeightLoss on High Blood Pressurehttp://www.portalsaudebrasil.com/artigospsb/obes064.pdf