Dehydration, hypoglycemia, aldosterone & cortisol

MeSci

ME/CFS since 1995; activity level 6?
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These past two weeks, I've been stricken with migraines, again. Driven by pain, I researched and found a correlation between elevated NO and migraine. ( various causes for folks)
Very sorry to hear about the migraines. I was diagnosed with migraine in 2014, and they were getting increasingly frequent (although I'm not clear whether the diagnosis still stands as I got a different diagnosis for what I thought was a bad migraine last year), and it is vile.

Did the feverfew stop working for you? I am taking that, and (touch wood, cross everything) haven't had a migraine since, although that includes the period before it should have started working, so I can't be sure it wasn't something else that stopped them.
 

picante

Senior Member
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I've seen more about the side effects of taking NO donors, (body building sites), than medical papers. People report headaches and having to pee a lot.

Well there's this in the first NO article @MeSci linked:
Nitric oxide is produced through a specialised sub-loop of a cyclical series of biochemical reactions known as the ornithine cycle (also known as the urea cycle).

The ornithine cycle is active in hepatocytes (liver cells) and is the cycle through which the harmful ammonia produced through the breakdown of proteins is converted into urea which is then excreted through the urine.

This side loop is known as the citrulline-NO cycle and is active in cells where production of nitric oxide is required for the functions discussed previously.

So if the body was hell-bent on making NO, would it have to upregulate the urea cycle?
 

Crux

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Did the feverfew stop working for you? I am taking that, and (touch wood, cross everything) haven't had a migraine since

I took feverfew combined with B2 and magnesium about 10 yrs ago., and they worked for a time. I now believe my migraines have an infectious cause, and the bacteria have been dumping a bunch of NO that inflames my brain.

I really hope it continues to work for you!
 

ahmo

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Sheesh, sometimes I think we need a supplement exchange. Then I could get rid of all my excess Enz. Therapy MeB12, which rots my teeth and my guts, too (thanks to the mannitol and fructose).
Supp Xchg would be good. You might try using those Enzy tablets as transdermal, crushed into some grease.

Do you remember what brand extracts you took
Nutricology hypothalamus, Enzymatic Therapies Adrenegize adrenal extract , Ultra Glandulars Raw Pituitary
 

Violeta

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Well there's this in the first NO article @MeSci linked:


So if the body was hell-bent on making NO, would it have to upregulate the urea cycle?
In some cases, as far as I know, if you decrease the type of protein that is nitrogenous(purines), there will be less ammonia to be broken down and so therefore less NO. Some people don't break down the ammonia, and the ammonia causes problems that seem similar to NO problems. (I have to eat very little purines or I get headaches and everything else associated with eating them.)

The thing about upregulating the urea cycle is a tricky question, because the body does it as well as it can, it does as much as it can to break down ammonia, creating urea is the correct handling of ammonia. When that cycle isn't working correctly for one reason or another, ammonia simply won't get broken down, causing a lot of problems. There are ways you can encourage it, but I don't think it would speed up simply in order to create more NO.

But there are other sources, if the items mentioned earlier cause NO production and don't contain purines.

There has to be something that I am missing, though, because when I drink raw milk and eat raw cheese for protein I am technically on a low purine diet. However, my arterial pressure relaxes.

What am I missing?
 

Violeta

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I took feverfew combined with B2 and magnesium about 10 yrs ago., and they worked for a time. I now believe my migraines have an infectious cause, and the bacteria have been dumping a bunch of NO that inflames my brain.

EBV does trigger NO.

"Induction of inducible nitric oxide synthase by Epstein-Barr virus B95-8-derived LMP1 in Balb/3T3 cells promotes stress-induced cell death and impairs LMP1-mediated transformation"
 

Violeta

Senior Member
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So arginine is precursor to NO, would lysine somehow inhibit it?

http://jcb.rupress.org/content/144/3/427.full

Excess nitric oxide (NO) induces apoptosis of some cell types, including macrophages. As NO is synthesized by NO synthase (NOS) from arginine, a common substrate of arginase, these two enzymes compete for arginine. There are two known isoforms of arginase, types I and II. Using murine macrophage-like RAW 264.7 cells, we asked if the induction of arginase II would downregulate NO production and hence prevent apoptosis. When cells were exposed to lipopolysaccharide (LPS) and interferon-γ (IFN-γ), the inducible form of NOS (iNOS) was induced, production of NO was elevated, and apoptosis followed. When dexamethasone and cAMP were further added, both iNOS and arginase II were induced, NO production was much decreased, and apoptosis was prevented.
 

picante

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You might try using those Enzy tablets as transdermal, crushed into some grease.
Thanks, dear ahmo. I've given up MeB12 for the moment. Up until last week I was taking some liquid drops transdermally. I'm off all methyl donor supps except the Citicoline (and ALCar). I suppose that's what's driving my need for potassium, since I'm also taking AdB12.
 

picante

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There has to be something that I am missing, though, because when I drink raw milk and eat raw cheese for protein I am technically on a low purine diet. However, my arterial pressure relaxes.

What am I missing?
Beats me. I found this, which indicates that raw milk & cheese are higher in lysine. What would be the effect of increasing your lysine/arginine ratio?

Edit: LOL, just saw your post above. You're wondering the same thing.:cool:
 

adreno

PR activist
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4,841
There's a connection between angiotensin and nitric oxide. When angiotensin is low, nitric oxide goes high. That's also why angiotensin inhibitors drop blood pressure.

Of course, angiotensin stimulates the release of aldosterone, so that would be low, too.
 
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Gondwanaland

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How did you find out you had an enterovirus infection?


The articles I quoted talk about the signals to the hypothalamus, including cytokines. Do you know which cytokines were high for you?

I've just taken a look at my last 13 years of hormone tests, and I've only found one for aldosterone, which was mid-range in 2009. I have no renin tests.

My blood glucose is always 60 when I'm fasting, and usually 80 when I've had something to eat before going to the lab (say, 90-120 minutes before). It has been this way for as long as I've been getting tests (20 years). (I've had ME/CFS for 23 years, triggered by EBV.)

I found an insulin test from 2009 as well. The post-prandial insulin was measured in the noon saliva sample of a 24-hour cortisol test. No doubt I followed instructions and had a carby meal an hour before.
Fasting ˂3 [3-12 uIU/mL]
Post-prandial ˂3 [5-20 uIU/mL]

Strangely, they've marked only the second result as "depressed". I do not know how to interpret this low-glucose, low-insulin phenomenon. It's certainly not insulin resistance!
@Gondwanaland
Please le t me know if you can make any sense out of this
http://www.diabetes-epidemic.com/blog1/-functional-hypoglycemia-clinical-fact-or-fiction
 

roller

wiggle jiggle
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long tim eago i also looked into nitric oxide.
it certainly is an issue for me, or it was.
i thought, the problem was the breaking down enzym nitric oxide synthease, or something.
...and concluded for some reason SOD might help.
im unsure about the SOD and dont take it anymore.

almost all inflammation seems to trigger NO, as its a pathogen killer.
 

MeSci

ME/CFS since 1995; activity level 6?
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EBV does trigger NO.

"Induction of inducible nitric oxide synthase by Epstein-Barr virus B95-8-derived LMP1 in Balb/3T3 cells promotes stress-induced cell death and impairs LMP1-mediated transformation"
That study involves an extremely artificial situation and GM mice. I would not assume relevance to humans in vivo. It may be relevant, but is equally likely not to be.
 

MeSci

ME/CFS since 1995; activity level 6?
Messages
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Location
Cornwall, UK
So arginine is precursor to NO, would lysine somehow inhibit it?

http://jcb.rupress.org/content/144/3/427.full

Excess nitric oxide (NO) induces apoptosis of some cell types, including macrophages. As NO is synthesized by NO synthase (NOS) from arginine, a common substrate of arginase, these two enzymes compete for arginine. There are two known isoforms of arginase, types I and II. Using murine macrophage-like RAW 264.7 cells, we asked if the induction of arginase II would downregulate NO production and hence prevent apoptosis. When cells were exposed to lipopolysaccharide (LPS) and interferon-γ (IFN-γ), the inducible form of NOS (iNOS) was induced, production of NO was elevated, and apoptosis followed. When dexamethasone and cAMP were further added, both iNOS and arginase II were induced, NO production was much decreased, and apoptosis was prevented.
I wonder what 'murine macrophage-like RAW 264.7 cells' are?! o_O Again, this is a very artificial situation using mouse cells.
 

MeSci

ME/CFS since 1995; activity level 6?
Messages
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Location
Cornwall, UK
There's a connection between angiotensin and nitric oxide. When angiotensin is low, nitric oxide goes high. That's also why angiotensin inhibitors drop blood pressure.

Of course, angiotensin stimulates the release of aldosterone, so that would be low, too.
Here's some stuff about angiotensin.
 
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