Dehydration, hypoglycemia, aldosterone & cortisol

[picante]

For a long time, I've thought that my adrenal fatigue is really adrenal misregulation.

Many of my usual symptoms are those of low cortisol and low aldosterone, but I know from a cortisol saliva test that my cortisol can shoot up when I exercise. The problem is that what goes up doesn't come down -- for a day or two. After exercise, my polyuria is worse for a day (at least). And the high cortisol does not give me energy; it feels just like neuro-exhaustion.

It seems like I've finally discovered the connection between my immune system imbalance and these symptoms, although I'm going to need some cytokine tests to confirm it:

The PVN is considered to be the final common structure where numerous different inputs initiate a stress response. Cytokines from the immune system, neurotransmitters from the nervous system, input from the limbic system (emotions), and hormones from the endocrine system all converge to elicit a stress response from the HPA axis at the PVN.

There's a concept in neurology called the central integrative state, which basically states that the net output of a neurological structure is a summation of the excitatory inputs versus the inhibitory inputs. In other words, if a combination of stimulus from neurotransmitters, hormones, and cytokines all result in an excitatory state, the result will be an elevation of cortisol.

On the other hand, if the combined total input is that of an inhibitory response, the results will be a low output of cortisol. This is how someone can go directly to the adrenal exhaustion phase: If the total summation of inputs is inhibitory to the PVN, there will be a diminished adrenal response and low cortisol.

Using this model, there's no such thing as "adrenal fatigue." Rather, it's merely a lack of inputs that can generate an adequate adrenal response.

The following can excite the PVN and therefore contribute to high cortisol: insulin, acetylcholine, elevated epinephrine and norepinepherine, and Th2 cytokines (IL-4, IL-5 and IL-10).

The following can inhibit the PVN and therefore contribute to low cortisol: GABA, low epinephrine and norepinepherine, endothelial nitric oxide, interferon, tumor necrosis factor, and Th1 cytokines (IFG, IL-12, TNF).

On Stop the Thyroid Madness, there is a section called How Does Inflammation Inhibit Cortisol?

A dysfunctional immune system will signal for higher levels of certain cytokines while suppressing others. Certain cytokines such at TGF-B1 (Transforming Growth Factor Beta One) can inhibit not only cortisol secretion but also aldostersone secretion. Then you have cytokines such as TNF-a (Tumor Necrosis Factor Alpha) which can attach itself to ACTH receptors on the adrenal gland and prevent cortisol secretion. Elevated levels of TNF-a are strongly associated with low morning levels of cortisol.

Certain cytokines such as Interluekin-10 (IL-10) can keep other proinflammatory cytokines at bay while also signaling cortisol secretion. This cytokine in specific can become smothered in people who have adrenal fatigue by other cytokines from the TH1 side of the immune system, which are acting aggressively. One of the functions of IL-10 is to keep the pro-inflammatory cytokines from the TH1 from over reacting. When pro-inflammatory cytokines are not put in check they can run rampant.

Some researchers are even beginning to theorize that over time our HPA-axis will numb itself to certain cortisol signaling cytokines such as (IL-3) and (IL-6) in order to preserve our body from prolonged exposure to cortisol. Cytokines are also strongly linked to other symptoms that are generally attributed to low cortisol, things like iron dumping, sleep disturbances, low appetite, hair loss and muscle wasting.

 

[picante]

Lately I've been desperate to find some way to keep water in my body; I've been losing weight again, and it's mostly water. But I just learned that my years-long habit of just adding sea salt isn't the ticket:

Salt should be used sparingly due to very low Aldosterone Levels, which are inhibited even more by higher salt intake. People who are sodium-sensitive generally are well aware of their problem, as they quickly retain extra water when ingesting larger amounts of salt, or their blood pressure goes up, however there are those who respond the opposite, where for instance drinking a medium-sized glass of water saturated with common table salt will have them keep running to the bathroom some time later, with some individuals losing perhaps as much as 10-15 lb of water weight. This is similar to the opposing effect of simple sugar consumption on hypoglycemia versus hyperglycemia.

In such a case, the strategy is not to increase someone's salt intake (which would otherwise cause more dehydration), but to boost aldosterone levels, which will subsequently increase sodium retention. Nutritional factors such as choline, licorice, iron, Vitamin B1, and - to a small extent - Vitamin E can be used for that purpose, which should be matched to individual requirements. http://www.acu-cell.com/pna.html

Choline should be used with caution if there is a disposition for water retention (swollen hands or feet), since it boosts aldosterone activity, which in turn results in sodium retention. http://www.acu-cell.com/dis-hyp.html

 

[picante]

If anyone has suggestions on how to rehydrate, please post them.

Has anyone done immune rebalancing, and has it helped with your adrenal function?

I've started taking Citicoline, and I already take B1 and E. I don't tolerate licorice well. I'm trying a rehydration drink made of water, salt, maple syrup and fresh lime juice.

I start out my day weighing about 117 lbs., then by bedtime I'm around 120 lbs. Then I get up to pee 3-4 times and I wind up parched, even though I'm drinking 2 or more 12-oz. glasses of water/rehydration drink at night.

Nighttime is usually when I have low cortisol symptoms, too, such as hypoglycemia.

 

[roller]

coconut water probably one of the best electrolytic, hydrating drinks available (by nature)

 

[halcyon]

The only thing that has improved my symptoms of polyuria/dehydration and hypoglycemia has been to treat my underlying enterovirus infection. I don't think it has anything to do with adrenal function. When measured, my aldosterone and renin levels were actually quite high, almost abnormal. I believe the issue is with the hypothalamus. Low ADH output and dysregulation of blood sugar levels.

The only thing that I could do prior to this was drink 3+ liters of water a day and eat constant high protein/fat meals.

 

[Violeta]

The only thing that has improved my symptoms of polyuria/dehydration and hypoglycemia has been to treat my underlying enterovirus infection. I don't think it has anything to do with adrenal function. When measured, my aldosterone and renin levels were actually quite high, almost abnormal. I believe the issue is with the hypothalamus. Low ADH output and dysregulation of blood sugar levels.

The only thing that I could do prior to this was drink 3+ liters of water a day and eat constant high protein/fat meals.

What did you do to treat you underlying enterovirus infection? I understand and agree about the hypothalamus/dehydration part, but would you mind expanding on it's connection to hypoglycemia and needing to eat high protein/fat meals, because while that type of diet helps me in so many ways I run into difficulty after a couple of weeks. Thanks

 

[picante]

The only thing that has improved my symptoms of polyuria/dehydration and hypoglycemia has been to treat my underlying enterovirus infection.

How did you find out you had an enterovirus infection?

When measured, my aldosterone and renin levels were actually quite high, almost abnormal. I believe the issue is with the hypothalamus.

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

 

[ahmo]

Simplistic and possibly useless: adrenal glandular worked for me, when I could no longer tolerate licorice or low dose cortef. And if the problem is hypothalamus-centered, hypothalamus glandular also gave me near immediate relief from the worst of my symptoms at the time. I was certainly having aldosterone issues at the time, don't know about any of your other issues affecting me at the time.

 

[picante]

Thanks, @ahmo, I have some Standard Process dessicated adrenal. It might be a good idea to re-order, though, since the expiration date is July 2010! I also have something homeopathic called "Pineal Pituitary Hypothalamus Drops", which expires in July 2016.

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).

 

[picante]

I managed to scan the cortisol curve from the day I had the insulin results.

This was done the day after I went X-C skiing for 90 minutes (which I can no longer do), and I was having my period (I was 52). Either of those two things could trigger a day or two of migraine/nausea/exhaustion, so I was in bed. At the time, I didn't know this was post-exertional neuro-exhaustion. I was just trying to figure out what was happening with my adrenals to cause these horrid migraines.

IOW, it wasn't a "normal" day. Cortisol was off the chart at noon. My "normal day" cortisol is a blunted curve.

 

[MeSci]

Lately I've been desperate to find some way to keep water in my body; I've been losing weight again, and it's mostly water. But I just learned that my years-long habit of just adding sea salt isn't the ticket:

I haven't read all the messages yet, but is Acu-Cell a reliable site? I ask because on the page you linked to it says

low sodium can actually increase the risk for heart disease,
but reduces the risk for stroke, while high sodium, by reducing atherogenic
development (arterial clogging), decreases the risk for some types of heart
disease, however it dramatically raises the risk for stroke when potassium
levels fall below those of sodium.

What do they mean by potassium levels falling below those of sodium? Using the UK units, serum sodium should be 133-146 mmol per litre and serum potassium should be 3.5-5.3 mmol per litre, hence many times lower than sodium.

Re sodium causing water retention, this may be the case for some, but as a fellow-polyuric, I seem to just pass excessive sodium and fluid in urine (not just excess), thus ending up dehydrated and hyponatraemic (sometimes seriously hyponatraemic). As this problem appeared to be exacerbated by an ACE inhibitor, I guess that it is due to low aldosterone, and may be a lifelong renal salt wasting condition. (I have always craved salt.)

I am also hypertensive, and have avoided licorice because it can increase blood pressure.

Perhaps all will become clear when I read the rest of the thread tomorrow!

 

[picante]

What do they mean by potassium levels falling below those of sodium?

I agree that is not well phrased. Usually he's talking about the balance between two minerals, and what happens when one mineral gets too high relative to the other.

Re sodium causing water retention, this may be the case for some, but as a fellow-polyuric, I seem to just pass excessive sodium and fluid in urine (not just excess), thus ending up dehydrated and hyponatraemic (sometimes seriously hyponatraemic). As this problem appeared to be exacerbated by an ACE inhibitor, I guess that it is due to low aldosterone, and may be a lifelong renal salt wasting condition. (I have always craved salt.)

This is pretty much what he says about adding more salt: that for some people it will drive aldosterone even lower. I tend to think I have renal salt wasting, too. I didn't like much salt until my metabolism crashed from EBV. Then I started craving it.

I am also hypertensive, and have avoided licorice because it can increase blood pressure.

Wow! Can you have low aldosterone and hypertension? I didn't know that was possible. My BP was a steady 90/60 until I added salt, and then it went even higher from starting T3 (thyroid).

 

[picante]

coconut water probably one of the best electrolytic, hydrating drinks available (by nature)

I'm thinking of trying this:

 

[Crux]

Hi @picante ,

I've been reading myself to utter confusion about Nitric Oxide, (NO), and its effects.

I don't have a grip on it, but when it's Elevated from; Infections, intake of nitrates, arginine, or citrulline, it can cause problems.

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.

Although NO is a necessary compound/neurotransmitter, too much can be down right neurotoxic. ( I think its been causing my migraines too.)

Here are a few articles : one concerns Aldosterone, which can be stimulated with increased serum potassium, etc.

Another article is about elevated NO and ACE in a group of dehydrated folks. The third is about ACE.

https://en.wikipedia.org/wiki/Aldosterone
http://www.bjbms.org/archives/2007-1/33-36.pdf
https://en.wikipedia.org/wiki/Angiotensin-converting_enzyme

 

[halcyon]

What did you do to treat you underlying enterovirus infection?

Equilibrant, inosine, lamivudine, and amantadine so far.

would you mind expanding on it's connection to hypoglycemia and needing to eat high protein/fat meals, because while that type of diet helps me in so many ways I run into difficulty after a couple of weeks.

There are glucosensing neurons in the hypothalamus that are supposed to help control hypoglycemic counterregulation. My guess is that this response becomes blunted. High carb meals will cause large spikes in blood sugar and then large spikes in insulin. Blood sugar will then drop without adequate opposition and so we get reactive hypoglycemia basically. Fat and protein won't spike blood sugar as much thus not so much insulin response keeping blood sugar levels more stable without needing the brain to counter the insulin response as much.

 

[picante]

From the first article, https://en.wikipedia.org/wiki/Aldosterone

Serum potassium concentrations are the most potent stimulator of aldosterone secretion.

Since I'm now taking 1200-2100 mg of K per day, you would think I'd have higher aldosterone! I'd better get it tested. (Potassium actually makes me pee even more, though.)

Most steroidogenic reactions are catalysed by enzymes of the cytochrome P450 family.

I don't understand what all these enzymes do, but according to my Sterling report, I only have one snp that's homozygous: rs1056836 (CYP1B1 L432V).

 

[halcyon]

How did you find out you had an enterovirus infection?

Stomach biopsy test from Dr. Chia's lab and serology tests from ARUP Labs.

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

Sadly no I haven't had access to much cytokine testing.

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.

ME patients with OI tend to have normal renin and lower aldosterone levels according to one study. I'm not sure why mine were so high, though they were measured very early in my illness.

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.)

Yow, I think I would be in a coma if my BG slipped into the 60s. I start getting symptoms when I drop into the 70s.

I do not know how to interpret this low-glucose, low-insulin phenomenon.

That is strange.

 

[Violeta]

Equilibrant, inosine, lamivudine, and amantadine so far.


There are glucosensing neurons in the hypothalamus that are supposed to help control hypoglycemic counterregulation. My guess is that this response becomes blunted. High carb meals will cause large spikes in blood sugar and then large spikes in insulin. Blood sugar will then drop without adequate opposition and so we get reactive hypoglycemia basically. Fat and protein won't spike blood sugar as much thus not so much insulin response keeping blood sugar levels more stable without needing the brain to counter the insulin response as much.

Thanks for that explanation. I had not thought that the hypothalamus had anything to do with blood glucose levels. (Hypoglycemia was one of my first symptoms at onset of chronic fatigue.) But I definitely had the lack of vasopressin and did realize that was traceable to the hypothalamus. I need to look up the relationship between vasopressin and aldosterone.

At one point when I had been reading about this I remember seeing that dopamine was involved in the loop. I don't know if that means anything in this conversation or not, but thought I would mention it.

 

[halcyon]

Hypoglycemia was one of my first symptoms at onset of chronic fatigue.

Same here. I had a small attack the night before onset and then a large one the day of.

I need to look up the relationship between vasopressin and aldosterone.

They both help control water balance, but have differing effects on osmolarity. This video might be helpful.

 

[Violeta]

I just wanted to add that the difficulty I have with a high fat/protein low carb diet seems to have something with reduced potassium intake, so while it helps in some ways, some things get worse.