Stims like hordenine/or dmaa activate the sympathetic ns, I'm looking for "stims" that don't. Been researching cordyceps as it has adenosine analogues, and coffee as it binds to adenosine receptor sites... Any ideas?
Coffee still activates the SNS..but it also acts by antagonizing adenosine receptors in the brain. The major issue is that it does nothing to increase Ado metabolism. So when caffeine is metabolized, you have a ton of Ado floating around waiting to bind receptors. Additionally, you get an upregulation of Ado receptors with caffeine use (tolerance).
And as for other stims... you'd be hard pressed to find a stimulant that doesn't have some sort of effect on the SNS/Adrenal axis.
Yes, that's why I'm looking for "least worst". T3 supplementation would be along thesr lines yes?
Yes but at least thyroid doesn't suppress the immune system as some other supplemental hormones such as corticosteroids.Originally Posted by ZiR RED
Personally I believe adrenal fatigue is a symptom of hypothyroidism, and also that chronic elevation of adrenaline, epinephrine, and cortisol are unhealthy (although they feel very good short term)Originally Posted by Bnatural
Yes I'm looking into those as well, thanks. I've tried the above and its hit or miss. I ordered some noopept to try (its a semi-racetam)Originally Posted by mr.cooper69
Endocr Pract. 2011 Jan-Feb;17(1):85-90.
Autoimmune hyperthyroidism due to secondary adrenal insufficiency: resolution with glucocorticoids.
Skamagas M, Geer EB.
Department of Medicine, Division of Endocrinology, Metabolism, and Bone Diseases, Mount Sinai School of Medicine, New York, New York, USA. email@example.com
To describe the course of autoimmune hyperthyroid disease in a patient with corticotropin (ACTH) deficiency treated with glucocorticoids.
We report the clinical presentation, laboratory data, imaging studies, and management of a patient with weight loss, fatigue, apathy, hallucinations, and arthritis.
Autoimmune hyperthyroidism (positive thyroperoxidase and thyroglobulin antibodies and borderline positive thyrotropin receptor antibody) was diagnosed in a 71-year-old woman. New psychotic symptoms prompted brain magnetic resonance imaging, which revealed a partially empty sella. Undetectable morning cortisol, undetectable ACTH, and failure to stimulate cortisol with synthetic ACTH (cosyntropin 250 mcg) secured the diagnosis of long-standing secondary adrenal insufficiency. Hydrocortisone replacement improved the patient's symptoms, resolved the thyroid disease, and decreased thyroid antibody titers. In retrospect, the patient recalled severe postpartum hemorrhage requiring blood transfusion at age 38 years. A Sheehan event probably occurred 33 years before the patient presented with corticotropin deficiency. Hyperthyroidism accelerated cortisol metabolism and provoked symptoms of adrenal insufficiency.
The hypocortisolemic state may precipitate hyperimmunity and autoimmune thyroid disease. Rapid resolution of hyperthyroidism and decreased thyroid antibody titers with glucocorticoid treatment support this hypothesis.
PMID:20841313 [PubMed - indexed for MEDLINE]Endocr Pract. 2006 Sep-Oct;12(5):572.
Reversible subclinical hypothyroidism in the presence of adrenal insufficiency.
Abdullatif HD, Ashraf AP.
Department of Pediatrics, Division of Pediatric Endocrinology and Metabolism, The Children's Hospital of Alabama, University of Alabama School of Medicine, Birmingham, Alabama 35233, USA.
To describe 3 different scenarios of reversible hypothyroidism in young patients with adrenal insufficiency.
We present 3 case reports of patients with adrenal insufficiency--one with delayed puberty, the second with type 1 diabetes and poor weight gain, and the third with hypoglycemia-related seizures and glucocorticoid deficiency--who had biochemical evidence of hypothyroidism.
Our first patient (case 1) initially had a mildly elevated thyrotropin (thyroid-stimulating hormone or TSH) level and a normal free thyroxine (FT4) level that, on follow-up assessment, had progressed to persistent mild elevation of TSH and low FT4 concentration. The other 2 patients (cases 2 and 3) had low FT4 and mildly elevated TSH values at the time of diagnosis of adrenal insufficiency. In all 3 patients, the results of thyroid function tests normalized with use of physiologic doses of adrenal hormone replacement therapy, without thyroid hormone replacement. All 3 patients remained euthyroid after 4, 3, and 1 year of follow-up, respectively.
These observations add insights into the complexities of the thyroadrenal interactions. These examples are important because thyroid hormone replacement in the setting of adrenal insufficiency could be unwarranted.
PMID:17002934 [PubMed - indexed for MEDLINE]
I'm not denying that adrenal overuse and burnout can occur in any number of metabolic states. However those rare (and lucky) hyper thyroid individuals tend to just need more nutrients, esp. Vit a. When an individual is hypo, sub clinical hypo, or auto immune hypo, usually their adrenaline/epinephrine/cortisol chemicals have been chronically used up as their body attempted to jury rig the failing system. By the time the wheels have fallen off, there's not enough juice left to cover up all the problems, and hopefully this leads to a proper diagnosis of hypo. Sadly though, esp if someone is sub clinical, they will be diagnosed with adrenal fatigue and given prednisone or cortisone, which will hurt them long term and not address the upstream cause.
Care to provide some research to elaborate and substantiate? I'm not doubting, but all I can find are whack doctors and nutritionists trying to sell books and supplements and making poorly substantiated claims.
Research is very poor in this area. If you work with these clients or suffer from the same issues you will have plenty of data. If you don't then it just becomes a vague myth "out there". This isn't about supplements, because one of the best ways to heal "adrenal fatigue" is with proper diet and t3. Again, self-application gives the best data as waiting for properly executed studies and mainstream acceptance is often too long for those suffering now.Originally Posted by ZiR RED
this thread is getting interesting.
are you still looking for insight on the topic?
it's good that you have counter arguments as it shows you don't just take the first suggestion and run, but some of your logic seems to somewhat flawed.
Further, application of thyroid hormone or hyperthyriodism appears to promote adrenal insufficiency. Here we see that T3 blocks down steam signalling by ACTH and compromises steroidalgenesis in the adrenal glands.
Am J Physiol. 1998 Feb;274(2 Pt 1):E238-45.
Acute effects of thyroid hormones on the production of adrenal cAMP and corticosterone in male rats.
Lo MJ, Kau MM, Chen YH, Tsai SC, Chiao YC, Chen JJ, Liaw C, Lu CC, Lee BP, Chen SC, Fang VS, Ho LT, Wang PS.
Department of Physiology, National Yang-Ming University, Taipei, Taiwan, Republic of China.
The acute effects of thyroid hormones on glucocorticoid secretion were studied. Venous blood samples were collected from male rats after they received intravenous 3,5,3'-triiodothyronine (T3) or thyroxine (T4). Zona fasciculata-reticularis (ZFR) cells were treated with adrenocorticotropic hormone (ACTH), T3, T4, ACTH plus T3, or ACTH plus T4 at 37 degrees C for 2 h. Corticosterone concentrations in plasma and cell media, and also adenosine 3',5'-cyclic monophosphate (cAMP) production in ZFR cells in the presence of 3-isobutyl-1-methylxanthine, were determined. The effects of thyroid hormones on the activities of steroidogenic enzymes of ZFR cells were measured by the amounts of intermediate steroidal products separated by thin-layer chromatography. Administration of T3 and T4 suppressed the basal and the ACTH-stimulated levels of plasma corticosterone. In ZFR cells, both thyroid hormones inhibited ACTH-stimulated corticosterone secretion, but the basal corticosterone was inhibited only with T3 > 10(-10) M or T4 > 10(-8) M. Likewise, T3 or T4 at 10(-7) M inhibited the basal- and ACTH-stimulated levels of intracellular cAMP. Physiological doses of T3 and T4 decreased the activities of 3 beta-hydroxysteroid dehydrogenase, 21-hydroxylase, and 11 beta-hydroxylase. These results suggest that thyroid hormones counteract ACTH in adrenal steroidogenesis through their inhibition of cAMP production in ZFR cells.
PMID:9486153 [PubMed - indexed for MEDLINE]
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I hate the term "adrenal fatigue", it just makes absolutely no sense to us it plus gives the illusion that all one needs to do is allow their adrenals to "rest" and all will get better. HPA dysfunction (the way the problem should be describe) is a real problem some have
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Because adrenal fatigue is probably thyroid fatigue. But a person would need to check their thyroid status. And judo josh is right on, thinking that just "resting" will somehow restore ppl is funny. We are also talking about different populations, probably most on this forum are in above average health, genetically and socially lucky.Originally Posted by Bnatural