Aldosterone Causes Fat Gain, Sodium May Prevent It

Koveras

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In confirmation of what @haidut said here

Salt Prevents Weight Gain On High Fat Diet

These researchers have shown that blocking Aldosterone, in this case with a receptor blocker, prevents fat gain on a high fat diet. The same effect of reducing aldosterone signalling, may be achievable more safely and practically with a high sodium intake

A novel combined glucocorticoid-mineralocorticoid receptor selective modulator markedly prevents weight gain and fat mass expansion in mice fed a h... - PubMed - NCBI

"BACKGROUND:
We have previously shown that antagonism of the mineralocorticoid receptor (MR) results in a potent antiadipogenic activity, in vitro and in vivo
. Excessive glucocorticoid exposure is associated with obesity and related disorders in humans and mice.

METHODS:
In this study, responses to a novel combined glucocorticoid receptor (GR)/MR antagonist were investigated in a model of diet-induced obesity. Female 10-week-old C57BL/6J mice were fed with normal chow or a high-fat diet (HFD) for 9 weeks. Mice fed a HFD were concomitantly treated for 9 weeks with the GR antagonist mifepristone (80 mg kg-1 per day) or the novel combined GR/MR antagonist CORT118335 (80 mg kg-1per day). Male, juvenile 6-week-old C57BL/6J mice fed HFD were treated with CORT118335 for 4 weeks.

RESULTS:
Mice fed a HFD showed a significant increase in total body weight and white fat mass, with impaired glucose tolerance and increased fat infiltration in livers. Interestingly, only CORT118335 completely prevented the HFD-induced weight gain and white fat deposition, whereas mifepristone showed no effect on body weight and modestly increased subcutaneous fat mass. Importantly, food intake was not affected by either treatment, and CORT118335 dramatically increased PGC-1α protein expression in adipose tissue, without any effect on UCP1. Both CORT118335 and mifepristone produced metabolic benefit, improving glucose tolerance, increasing adiponectin plasma levels, decreasing leptin and reducing mean adipocyte size. When tested in vitro, CORT118335 markedly reduced 3T3-L1 differentiation and reversed MR-mediated pro-adipogenic effects of aldosterone; differently, GR-mediated effects of dexamethasone were not antagonized by CORT118335, suggesting that it mostly acts as an antagonist of MR in cultured preadipocytes.

CONCLUSIONS:
Combined GR/MR pharmacological antagonism markedly reduced HFD-driven weight gain and fat mass expansion in mice through the increase in adipose PGC-1α, suggesting that both receptors represent strategic therapeutic targets to fight obesity. The effects of CORT118335 in adipocytes seem predominantly mediated by MR antagonism.
 

CoolTweetPete

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Thanks for this.

Medicine is bordering on criminal negligence recommending low salt intake. I've tried to convince my dad that salt is critical to health, but I'm not wearing a white jacket when I say it, so he pops his blood pressure meds and ignores me.
 

haidut

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In confirmation of what @haidut said here

Salt Prevents Weight Gain On High Fat Diet

These researchers have shown that blocking Aldosterone, in this case with a receptor blocker, prevents fat gain on a high fat diet. The same effect of reducing aldosterone signalling, may be achievable more safely and practically with a high sodium intake

A novel combined glucocorticoid-mineralocorticoid receptor selective modulator markedly prevents weight gain and fat mass expansion in mice fed a h... - PubMed - NCBI

"BACKGROUND:
We have previously shown that antagonism of the mineralocorticoid receptor (MR) results in a potent antiadipogenic activity, in vitro and in vivo
. Excessive glucocorticoid exposure is associated with obesity and related disorders in humans and mice.

METHODS:
In this study, responses to a novel combined glucocorticoid receptor (GR)/MR antagonist were investigated in a model of diet-induced obesity. Female 10-week-old C57BL/6J mice were fed with normal chow or a high-fat diet (HFD) for 9 weeks. Mice fed a HFD were concomitantly treated for 9 weeks with the GR antagonist mifepristone (80 mg kg-1 per day) or the novel combined GR/MR antagonist CORT118335 (80 mg kg-1per day). Male, juvenile 6-week-old C57BL/6J mice fed HFD were treated with CORT118335 for 4 weeks.

RESULTS:
Mice fed a HFD showed a significant increase in total body weight and white fat mass, with impaired glucose tolerance and increased fat infiltration in livers. Interestingly, only CORT118335 completely prevented the HFD-induced weight gain and white fat deposition, whereas mifepristone showed no effect on body weight and modestly increased subcutaneous fat mass. Importantly, food intake was not affected by either treatment, and CORT118335 dramatically increased PGC-1α protein expression in adipose tissue, without any effect on UCP1. Both CORT118335 and mifepristone produced metabolic benefit, improving glucose tolerance, increasing adiponectin plasma levels, decreasing leptin and reducing mean adipocyte size. When tested in vitro, CORT118335 markedly reduced 3T3-L1 differentiation and reversed MR-mediated pro-adipogenic effects of aldosterone; differently, GR-mediated effects of dexamethasone were not antagonized by CORT118335, suggesting that it mostly acts as an antagonist of MR in cultured preadipocytes.

CONCLUSIONS:
Combined GR/MR pharmacological antagonism markedly reduced HFD-driven weight gain and fat mass expansion in mice through the increase in adipose PGC-1α, suggesting that both receptors represent strategic therapeutic targets to fight obesity. The effects of CORT118335 in adipocytes seem predominantly mediated by MR antagonism.


Thanks for this. Btw, Ray said that progesterone is the safest aldosterone antagonist and it is probably the most potent as well, barring any chemical monstrosity created by the pharma goons.
 

800mRepeats

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My first thought on reading Koveras's post was "progesterone!" - thanks for mentioning it Haidut.

I recently had an experience right after trying Progestene that's made me wonder about the progesterone--aldosterone link ...
My question is, could blocking aldosterone cause muscle cramping?
 

haidut

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My first thought on reading Koveras's post was "progesterone!" - thanks for mentioning it Haidut.

I recently had an experience right after trying Progestene that's made me wonder about the progesterone--aldosterone link ...
My question is, could blocking aldosterone cause muscle cramping?

Well, if you block aldosterone but do not increase salt intake then you will lose salt and of course can get cramping. Aldosterone rises to keep sodium, and it does at the expense of magnesium and potassium. So, blocking aldosterone has to go hand in hand with increasing sodium intake. But if you increase sodium intake you won't have to block aldosterone as it won't rise to start with :):
 

800mRepeats

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Thank you, Haidut. That's helpful.

And, I see that over the past 6 months my sodium intake has gone from about 2400mg to 3200mg / day - no idea whether this is enough, too much, or too little. That's just salting to taste (with minimal processed *food* in my diet - cheese is about as fancy as it gets).
 

dfspcc20

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Medicine is bordering on criminal negligence recommending low salt intake. I've tried to convince my dad that salt is critical to health, but I'm not wearing a white jacket when I say it, so he pops his blood pressure meds and ignores me.

I've seen my mom's health decline in so many areas, which I attribute mostly to the low-sodium diet her doctors have convinced her is necessary for her Meniere's disease. Low sodium diet + diuretics lead to heart palpitations. So they give her a potassium supplement (!). Then terrible sleep, not being able to handle temps outside over 80 deg F, declining mental and physical function, scary blood-pressure issues. Then finally the diagnosis of "hyperaldosteronism"- do the doctors consider that they directly caused this. Nope! Here's some more medications to deal with these symptoms. And all the studies and advice I give her is just met with "that's cute, but why don't they see that in the blood tests?" #facepalm
 

superhuman

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@haidut But if aldosterone is high and you increase salt, that will leave you with water retention right? how long does it take for increased salt intake starts to lower aldosterone?
 

haidut

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@haidut But if aldosterone is high and you increase salt, that will leave you with water retention right? how long does it take for increased salt intake starts to lower aldosterone?

Usually immediately. Aldosterone release is very sensitive to serum sodium levels and that is why most doctors do not want to test aldosterone on a blood test if it's only a single test. It can change values drastically in a matter of minutes. Water retention is from estrogen and energetic failure, not from sodium.
 

YuraCZ

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Thank you, Haidut. That's helpful.

And, I see that over the past 6 months my sodium intake has gone from about 2400mg to 3200mg / day - no idea whether this is enough, too much, or too little. That's just salting to taste (with minimal processed *food* in my diet - cheese is about as fancy as it gets).
I don't eat anything with added sodium. But I add 1/2 tsp of sea salt to every 600ml of water( I drink about 3,5l a day) + 1 really full tsp to every meal ( I eat 3 meals per day) So it is A LOT of sodium I guess.. :)
 

tankasnowgod

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@haidut Cool. But when me or others raise their sodium intake and get more water retention? why does that happen then?

I think increased sodium can cause temporary water retention, and it may take a week or two for the body to normalize. It's well known among people that want to cut weight massively and temporarily can achieve this by altering salt, water, and carbohydrate intake. If you search "cutting water weight," you can find some of these strategies.
 

Milena

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I will put this in the bag to try later (not too many variables at once)
I probably have high aldosterone as my consultant put me on spironolactone as I had high blood pressure and salty skin (salt wasting, I now understand) even If I wasn't hot or even mildly warm. My cats loved licking me :)
 

tomisonbottom

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I will put this in the bag to try later (not too many variables at once)
I probably have high aldosterone as my consultant put me on spironolactone as I had high blood pressure and salty skin (salt wasting, I now understand) even If I wasn't hot or even mildly warm. My cats loved licking me :)

Are you still on spiro?

I think it raises estrogen.
 

Bart1

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Well, if you block aldosterone but do not increase salt intake then you will lose salt and of course can get cramping. Aldosterone rises to keep sodium, and it does at the expense of magnesium and potassium. So, blocking aldosterone has to go hand in hand with increasing sodium intake. But if you increase sodium intake you won't have to block aldosterone as it won't rise to start with :):
@haidut
I hope you could give some insight.
If one uses progesterone to lower cortisol. How would one approach the sodium intake. Upping sodium intake has been correlated with an increase in cortisol right? however progesterone, since being an aldosterone antagonist requires salt as you state here. I’m asking because since using progesterone I seem to have more fluid rentention however increasing sodium gives me (sometimes )also stress...
 

Owen B

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I'm confused about the salt/aldosterone relationship.

I have what looks like the three symptoms associated with high aldosterone: excessive urination (and salivation), heart arrhythmias and muscle cramps. But I was already using a lot of salt. I stopped the salt cold and the intensity of the arrhythmias decreased 90%, the muscle cramps disappeared almost completely. I still have what seems like excessive urination.

I thought salt is supposed to inhibit aldosterone.

What am I missing here? Thyroid?
 

lampofred

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I'm confused about the salt/aldosterone relationship.

I have what looks like the three symptoms associated with high aldosterone: excessive urination (and salivation), heart arrhythmias and muscle cramps. But I was already using a lot of salt. I stopped the salt cold and the intensity of the arrhythmias decreased 90%, the muscle cramps disappeared almost completely. I still have what seems like excessive urination.

I thought salt is supposed to inhibit aldosterone.

What am I missing here? Thyroid?

I don't think increasing sodium intake is the optimal way to reduce aldosterone. CO2 production is what naturally retains sodium, so if you are producing a lot of CO2, you need to consume very little salt to suppress aldosterone, whereas if you are not producing a lot of CO2, then even if you consume large quantities of salt you will still be producing excess aldosterone because you will not be retaining the salt you consume.
 

lampofred

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@haidut
I hope you could give some insight.
If one uses progesterone to lower cortisol. How would one approach the sodium intake. Upping sodium intake has been correlated with an increase in cortisol right? however progesterone, since being an aldosterone antagonist requires salt as you state here. I’m asking because since using progesterone I seem to have more fluid rentention however increasing sodium gives me (sometimes )also stress...

Progesterone is an aldosterone "antagonist" because it has the same functions as aldosterone but to a milder degree. So it is not technically an antagonist. In a sense aldosterone is just a lower quality replacement hormone for when progesterone is not produced sufficiently.

The reason progesterone is a bit milder than aldosterone is that endogenous progesterone production is also accompanied by high CO2 production, and CO2 has also has sodium retaining properties like progesterone. So the situations are:

Best case (in health): high progesterone (mild sodium retention) + high CO2 (mild sodium retention) = strong sodium retention
Backup scenario (in stress): progesterone and CO2 production fails but aldosterone on its own is a strong sodium retainer so result = strong sodium retention
Your scenario: artificial progesterone supplementation (mild sodium retention) + aldosterone antagonism by progesterone + low CO2 production = not enough sodium retention hence the fluid retention

Increasing salt consumption won't help because with low CO2, you will just dump the salt. So the trick is to increase CO2, by constant bag breathing, thyroid, etc.
 
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