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Adrenal problems after synthroid treatment

Hi Dr. Mark,
I have a theory question.

I stopped by here last year, very ill after starting thyroxine-TSH 200.   Symptoms were salt wasting and excessive urination leading to joint/muscle pain, headaches, nausea, blue numb hands and feet and eventually bouts of delirium when I drank water or electrolytes.  3 endos all agree that it looked adrenal but adrenal tests were all normal. No one has any answers.  I got better after taking florinef when starting the synthroid and rapidly improved.  Another lady also posted on the board with the exact same set of symptoms.

Importantly-no pretreatment edema at all- likely due to the protective effects of a collagen disorder (EDS III).   Reduced interstitial space I believe thus much less water and poly saccaride buildup. see through skin, reduced skin thickness and so on.

I think my brain thought it needed to dump water and salt due to the sudden drop in TSH but my body didn
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Avatar universal
Hi ACTH,

I think the cortisol extracts may be okay for many people but when you hang around some of the adrenal groups on the web long enough you'll find people do some crazy stuff.  One guy would take 60 mg of prednisone for 1 month then stop abruptly in an attempt to combat chronic fatigue.  That would kill many people.  

So it's the same idea with the cortisol or extracts.  They likely work okay for many-most people but the worry is that the more "off" and unstable your endocrine system is the more likely you might make yourself really ill by taking them.  So us folks who have the adrenal symptoms may be the ones most likely to get ill by taking even small doses of adrenal extracts.  I am so happy that you guys are all doing well on the extracts but I just urge being very careful if you chose to go in that direction.  Endos are really not helpful here because we are outliers from a health perspective.  There are not many of us that present with these symptoms and they don't always know what to do about it.

Sorry I got a little technical in the above post!  I am guessing you know that your brain releases CRH (cortisol releasing hormone)in the hypothalumus.  That goes down to the pituatary and causes ACTH to be released.  Then that goes to your adrenal gland to stimulate cortisol production.  So according to traditional views-the stuff your endo knows-if there is a problem it is in that pathway somewhere.

There is a ton of work indicating that irregularities in the HPA axis (the above pathway) can cause depression and chronic fatigue symptoms and from talking with many folks here it seems that this crosses into more standrard endocrinology in the adrenal fatigue problems that arise after treating other endocrine problems.

I spent months looking at the above pathway in terms of what was wrong with me and many of you guys and it was likepieces were missing.  It just didn't add up so cleanly.   Then I found the papere in the original link-it's a free download if you follow the links.  

It appears that ACTH release is also controlled by ADH (antidiuretic hormone)/AVP (arginine vasopressine).  This little hormone, according to endos, controls how much water your body keeps in.  read about diabetes insipidus or SIADH as those are the standard disorders endos run into involving ADH.  

But the paper says it also plays a role in regulating ACTH production thus adding a whole extra-complicated-addition to how cortisol secretion is controlled.  Most endos don't even know the pathway exists so are not in a position to understand how it might effect the HPA axis.  They don't really have time to think like scientists as they are kept really busy with pateints due to the shortage of endos nationwide.

Most of the time the role of ADH is pretty silent.  Obvious problems have been found at all points in the CRH-ACTH-cortisol pathway but I don't think it is until your system is really messed up that you might see the role ADH is playing in coregulation.  Like some of us here!

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Avatar universal
A related discussion, marilyn was started.
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Avatar universal
Florinef, I got lost in the technicalities...would you be willing to simplify a bit?

First, are you saying that no one should take adrenal extracts, or just those with similar conditions?

Are you also saying that physiologic doses of hydrocortisone are not appropriate, or just that within the adrenal extracts?

Is this a feedback loop you're referring to?  Please expand...in layman's terms simple enough for a hypobrain!  :)

Thanks!
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Avatar universal
I wanted to post my ideas on the above topic a bit further.  They seemed to explain some very bad times I went through when none of the 20 some odd doctors I saw could figure out what was wrong. A couple of oddities below.  Maybe they can help someone else who gets stuck where I did.   I was going to kill myself this last summer because I couldn
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Avatar universal
Ultradian, circadian, and stress-related hypothalamic-pituitary-adrenal axis activity--a dynamic digital-to-analog modulation.
Endocrinology. 1998 Feb;139(2):437-40. Review. No abstract available.
PMID: 9449607 [PubMed - indexed for MEDLINE]

Sorry, here's that ref.  It's pretty old but when I stumbled across it it made me rethink my med combination substantially as well as all the problems I had been having.

Also, remember Ar who got orthostatic hypotension after large doses of cortisol and florinef wasn't helping much?   Something like that happened to me as well later on due to a very small 5 mg dose of cortisol.  Perhaps the same type of problem?
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97953 tn?1440865392
MEDICAL PROFESSIONAL
Adrenal insufficiency sx are different from DI sx that would be the result of a transient drop in ADH -- ADH comes from posterior pituitary, whereas TSH from the anterior.  I do not know of any definite link b/w TSH and ADH.  THe CRH/ACTH link may make more sense b/c of the ADH effect on salt/fluid that is governed in part by the adrenal -- however this effect (mineralocorticoid) is not governed by ACTH in the way that glucorticoid production is.  So, interesting question.

The fluid retention seen in severe hypo is linked to decreased renal function due to low thyroid. Correcting this mobilizes fluid due to improved kidney filtration. I don't think it is ADH mediated.
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