Acute ebv reactivation and dhea

[godlovesatrier]

Thought I'd post about this ij case it's useful for anyone else.

Woke up with a sore throat two days ago and had crashed. Physical fatigue with a general unwell feeling. Pushed through that becuase I'm moving house and didn't really have any choice. Throat became progressively more and more sore until midday when I noticed my tonsils were very swollen.

By this point I didn't realise but there seemed to be a run away effect already. I felt very wired and I know realise this is an inflammatory response. Where the body can't switch off and has got stuck in an "on" state.

My tongue is also a bit swollen, I've been sneezing a little, some mucous and phlegm production, slight cough, nose is sore inside and stuffy. All symptoms I know are ebv related. I did do a lateral flow which was negativer. I'm confident it's not covid.

I took 500mg valtrex twice yesterday but this only reduced the pain and swelling for an hour. Which made me question whether it was ebv.

Last time I was in hospital my ebv didn't actually respond to rest or killing the bacteria in my tonsils (I had a throat infection too) straight away. I had to go back the day after and get help again because the swelling wasn't going down. They gave me steroids by iv and then everything started to feel better.

So last night I was really panicking. I know I couldn't take hydrocortisone becuase the doses are immune suppressive and we have a big wave of covid here right now.
So I googled dhea as a steroid hormone/to see if it could raise cortisol and found plenty of studies showing it was very anti inflammatory.
I took 50mg and waited ten minutes. 20 minutes in the swelling went down. I took another 50mg and 3 drops of pregnenolone (which may not have been as anti inflammatory) and the swelling reduced again by about 75%.

I also don't have any fatigue thismorning. And I'm like how is that even possible. I've never been dhea deficient btw. Tests are always bang on mid range. But maybe t levels are part of the reason I have ME? I got four hours sleep. So maybe that's long enough for 100mg dhea to convert to t.

The thing is. Ill be getting a blood test tomorrow for hormones. I'll have to see if it's gone up after I get it.

Very relieved about my tonsils. But still feel a bit wired. Hoping it stays as it is.

I think I'll have to take dhea with the valtrex today.

Advise welcome and ideas about the dhea making my fatigue better also v welcome. Never heard of anyone but Heaps getting anything from dhea.

Cheers.

 

[CSMLSM]

Thought I'd post about this ij case it's useful for anyone else.

Woke up with a sore throat two days ago and had crashed. Physical fatigue with a general unwell feeling. Pushed through that becuase I'm moving house and didn't really have any choice. Throat became progressively more and more sore until midday when I noticed my tonsils were very swollen.

By this point I didn't realise but there seemed to be a run away effect already. I felt very wired and I know realise this is an inflammatory response. Where the body can't switch off and has got stuck in an "on" state.

My tongue is also a bit swollen, I've been sneezing a little, some mucous and phlegm production, slight cough, nose is sore inside and stuffy. All symptoms I know are ebv related. I did do a lateral flow which was negativer. I'm confident it's not covid.

I took 500mg valtrex twice yesterday but this only reduced the pain and swelling for an hour. Which made me question whether it was ebv.

Last time I was in hospital my ebv didn't actually respond to rest or killing the bacteria in my tonsils (I had a throat infection too) straight away. I had to go back the day after and get help again because the swelling wasn't going down. They gave me steroids by iv and then everything started to feel better.

So last night I was really panicking. I know I couldn't take hydrocortisone becuase the doses are immune suppressive and we have a big wave of covid here right now.
So I googled dhea as a steroid hormone/to see if it could raise cortisol and found plenty of studies showing it was very anti inflammatory.
I took 50mg and waited ten minutes. 20 minutes in the swelling went down. I took another 50mg and 3 drops of pregnenolone (which may not have been as anti inflammatory) and the swelling reduced again by about 75%.

I also don't have any fatigue thismorning. And I'm like how is that even possible. I've never been dhea deficient btw. Tests are always bang on mid range. But maybe t levels are part of the reason I have ME? I got four hours sleep. So maybe that's long enough for 100mg dhea to convert to t.

The thing is. Ill be getting a blood test tomorrow for hormones. I'll have to see if it's gone up after I get it.

Very relieved about my tonsils. But still feel a bit wired. Hoping it stays as it is.

I think I'll have to take dhea with the valtrex today.

Advise welcome and ideas about the dhea making my fatigue better also v welcome. Never heard of anyone but Heaps getting anything from dhea.

Cheers.

I may be able to help

Effects of androgens and estrogens on sirtuin 1 gene expression in human aortic endothelial cells - PMC (nih.gov)
Conclusion:
These results suggest that DHEA, androstenedione, testosterone, E1, and E2 definitely activate SIRT1 expression in HAECs. A high glucose medium is potent to inhibit the basal gene expression; however, it could not reduce powerful androgen- and estrogen-induced SIRT1 expression in HAECs.


From Wiki-
Lipid metabolism is the synthesis and degradation of lipids in cells, involving the breakdown or storage of fats for energy and the synthesis of structural and functional lipids, such as those involved in the construction of cell membranes.


SIRT1 promotes lipid metabolism and mitochondrial biogenesis in adipocytes and coordinates adipogenesis by targeting key enzymatic pathways | Scientific Reports (nature.com)
Abstract
The NAD+-dependent deacetylase SIRT1 controls key metabolic functions by deacetylating target proteins and strategies that promote SIRT1 function such as SIRT1 overexpression or NAD+ boosters alleviate metabolic complications. We previously reported that SIRT1-depletion in 3T3-L1 preadipocytes led to C-Myc activation, adipocyte hyperplasia, and dysregulated adipocyte metabolism. Here, we characterized SIRT1-depleted adipocytes by quantitative mass spectrometry-based proteomics, gene-expression and biochemical analyses, and mitochondrial studies. We found that SIRT1 promoted mitochondrial biogenesis and respiration in adipocytes and expression of molecules like leptin, adiponectin, matrix metalloproteinases, lipocalin 2, and thyroid responsive protein was SIRT1-dependent. Independent validation of the proteomics dataset uncovered SIRT1-dependence of SREBF1c and PPARα signaling in adipocytes. SIRT1 promoted nicotinamide mononucleotide acetyltransferase 2 (NMNAT2) expression during 3T3-L1 differentiation and constitutively repressed NMNAT1 and 3 levels. Supplementing preadipocytes with the NAD+ booster nicotinamide mononucleotide (NMN) during differentiation increased expression levels of leptin, SIRT1, and PGC-1α and its transcriptional targets, and reduced levels of pro-fibrotic collagens (Col6A1 and Col6A3) in a SIRT1-dependent manner. Investigating the metabolic impact of the functional interaction of SIRT1 with SREBF1c and PPARα and insights into how NAD+ metabolism modulates adipocyte function could potentially lead to new avenues in developing therapeutics for obesity complications.

SIRT1: A Potential Therapeutic Target in Autoimmune Diseases - PMC (nih.gov)
Abstract
The morbidity and mortality of autoimmune diseases (Ads) have been increasing worldwide, and the identification of novel therapeutic strategies for prevention and treatment is urgently needed. Sirtuin 1 (SIRT1), a member of the class III family of nicotinamide adenine dinucleotide (NAD+)-dependent histone deacetylases, has been reported to participate in the progression of several diseases. SIRT1 also regulates inflammation, oxidative stress, mitochondrial function, immune responses, cellular differentiation, proliferation and metabolism, and its altered functions are likely involved in Ads. Several inhibitors and activators have been shown to affect the development of Ads. SIRT1 may represent a novel therapeutic target in these diseases, and small molecules or natural products that modulate the functions of SIRT1 are potential therapeutic agents. In the present review, we summarize current studies of the biological functions of SIRT1 and its role in the pathogenesis and treatment of Ads.

Sirt-1 activation is part of why I use Caryophyllene (in Copaiba essential oil) and supplement with Omega 3 capsules, see below-
Activation of type 2 cannabinoid receptors (CB2R) promotes fatty acid oxidation through the SIRT1/PGC-1α pathway - PubMed (nih.gov)
Abstract
Abnormal fatty acid oxidation has been associated with obesity and type 2 diabetes. At the transcriptional level, peroxisome proliferator-activated receptor-gamma coactivator 1α (PGC-1α) has been reported to strongly increase the ability of hormone nuclear receptors PPARα and ERRα to drive transcription of fatty acid oxidation enzymes. In this study, we report that a specific agonist of the type 2 cannabinoid receptor (CB2R) can lead to fatty acid oxidation through the PGC-1α pathway. We have found that CB2R is expressed in differentiated C2C12 myotubes, and that use of the specific agonist trans-caryophyllene (TC) stimulates sirtuin 1 (SIRT1) deacetylase activity by increasing the phosphorylation of cAMP response element-binding protein (CREB), thus leading to increased levels of PGC-1α deacetylation. This use of TC treatment increases the expression of genes linked to the fatty acid oxidation pathway in a SIRT1/PGC-1α-dependent mechanism and also drastically accelerates the rate of complete fatty acid oxidation in C2C12 myotubes, neither of which occur when CB2R mRNA is knocked down using siRNA. These results reveal that activation of CB2R by a selective agonist promotes lipid oxidation through a signaling/transcriptional pathway. Our findings imply that pharmacological manipulation of CB2R may provide therapeutic possibilities to treat metabolic diseases associated with lipid dysregulation.

The role of Peroxisome Proliferator-Activated Receptors (PPAR) in immune responses - PMC (nih.gov)
Abstract
Peroxisome proliferator-activated receptors (PPARs) are fatty acid-activated transcription factors of nuclear hormone receptor superfamily that regulate energy metabolism. Currently, three PPAR subtypes have been identified: PPARα, PPARγ, and PPARβ/δ. PPARα and PPARδ are highly expressed in oxidative tissues and regulate genes involved in substrate delivery and oxidative phosphorylation (OXPHOS) and regulation of energy homeostasis. In contrast, PPARγ is more important in lipogenesis and lipid synthesis, with highest expression levels in white adipose tissue (WAT). In addition to tissues regulating whole body energy homeostasis, PPARs are expressed in immune cells and have an emerging critical role in immune cell differentiation and fate commitment. In this review, we discuss the actions of PPARs in the function of the innate and the adaptive immune system and their implications in immune-mediated inflammatory conditions.


From Wiki-
Function
PPAR-α is a transcription factor regulated by free fatty acids, and is a major regulator of lipid metabolism in the liver.[7] PPAR-alpha is activated under conditions of energy deprivation and is necessary for the process of ketogenesis, a key adaptive response to prolonged fasting.[8][9] Activation of PPAR-alpha promotes uptake, utilization, and catabolism of fatty acids by upregulation of genes involved in fatty acid transport, fatty acid binding and activation, and peroxisomal and mitochondrial fatty acid β-oxidation.[10] Activation of fatty acid oxidation is facilitated by increased expression of CPR1 (which brings long-chain lipids into mitochondria) by PPAR-α.[11] PPAR-α also inhibits glycolysis, while promoting liver gluconeogenesis and glycogen synthesis.[7]

In macrophages, PPAR-α inhibits the uptake of glycated low-density lipoprotein (LDL cholesterol), inhibits foam cell (atherosclerosis) formation, and inhibits pro-inflammatory cytokines.[11]

Hope this is what you were asking for

 

[CSMLSM]

Dehydroepiandrosterone effects on the mRNA levels of peroxisome proliferator-activated receptors and their coactivators in human hepatoma HepG2 cells - PubMed (nih.gov)
To investigate the effect of dehydroepiandrosterone (DHEA) on intracellular mRNA levels of peroxisome proliferator-activated receptors (PPARs) and PPAR-gamma coactivators (PGCs), we conducted a quantitative real-time RT-PCR study using HepG2 cells. Treatment with 100 micromol/l DHEA for 2-20 h caused a time-dependent elevation of mRNA levels in the cells. Upon 20 h, PPAR-alpha, -gamma1, and -gamma2 mRNAs and PGC-1alpha and -1beta mRNAs increased to 157, 161, 155, 656, and 475% of control levels, respectively (p < 0.05 each). Treatment with actinomycin D for 2.5-8 h revealed a significant stabilization effect of DHEA on PPAR-gamma1 and PGC-1alpha mRNAs at both 2.5 and 8 h incubation periods and a mild but significant stabilization effect on PGC-1beta mRNA at the 8 h incubation period suggesting that DHEA can modulate turnover of these mRNA transcripts. Basal mRNA levels of PPAR-alpha and PGC-1alpha were significantly suppressed upon 20 h treatment with cycloheximide, while those of PPAR-gamma1, -gamma2, and PGC-1beta were elevated. Cycloheximide also significantly reduced DHEA-induced accumulation of PPAR-alpha, -gamma1, -gamma2, and PGC-1alpha mRNAs, demonstrating the dependence of the DHEA action on de novo protein synthesis. The findings demonstrate that a supraphysiological concentration of DHEA can substantially influence gene expression of the PPAR signalling machinery at both transcriptional and posttranscriptional levels.

 

[godlovesatrier]

Well it's definitely a steroid hormone. If you Google dhea and inflamation it comes up that dhea is a rather potent anti inflammatory. But I assume cortisol is the master anti inflammatory hormone.

Saying that I just meditated for ten minutes and thats also had an effect but not as good as the dhea of course.

I'd like to take 10mg hydrocortisone but I'm concernrd this will be immune suprressive. Although the UK drug website that doctor's use says that it's not at that dose. But I couldn't find another source to corroborate.

I feel better than I did thismorning. But I've had a busy isu day at work. I'm taking it easy.

But my tongue is very swollen and it hurts to talk a the moment. Typical ebv symptom. No doubt it's 100% ebv.

I've switched to 1g valtrex every 6 hours. 25mg dhea in the morning ideally and not at night. One andrographis dose in the am - which helped hugely but also brought on a slight temperature. Just praying I start to feel better. My body can't get sick until the weekend!

Stress is really screwing me over a the moment. I'm about to get a blood test for cortisol tomorrow. Be interesting to see what it shows.

 

[Judee]

For years, I took Dhea at a doctor's direction. When he "prescribed" it, he wanted me to start out with 10mg (IIRC). I choose to start at 5mg. He wanted me to then titrate up to 40mg (doubling my dose every week).

The first week I do think I felt better but the second week it made me feel angry.

I didn't like that so I went back down to 5mg a day and stayed there for probably 9 more years even though I don't think it ever did anything after that first week.

I kept asking the doctor if he thought I could ever go off of the hormones and he kept saying probably not.

Well, after that many years and the low doses I was taking, I started to go off of them.

One scary symptom I'd had and told him about was something I called "spiral down." Whenever I rolled onto my right side to sleep, it was like my energy was being instantly sucked down some invisible vortex...like water spiraling down a drain.

I would have to quickly roll back over to my left side.

For a year and a half I could only sleep on my left side because every time I tried to do the right side, I felt that. It took me years later to realize I was probably blacking out when that happened.

After I weaned off of most of the hormones he had me on (2 thyroid meds, iodine, and DHEA). I realized that awful symptom had gone away as well as the daily excruciating hypoglycemic episodes I'd been having.

I heard of one other person who mentioned this on healthrising in the comments on one article about what he speculated was happening to the heart and blood flow when we rolled onto the right side. I wish I had saved it. How he explained it made a lot of sense.

Anyway, I don't know why I rambled on so much about it. I guess just to say be careful with it and maybe watch for similar things happening.

Oh, and it also messed up my SHBG levels. Of course, I didn't find that out until I stopped going to him and had requested all my records. Oddly enough, he never went over those test results with me.

Thank the Lord, after I went off the DHEA my SHBG levels did return to normal. After that many years of using it, I was concerned they wouldn't.

 

[godlovesatrier]

Strange. it does sound anatomical. So heart makes sense. But how awful for you. Not nice at all!

They are strong hormones. Also I made a typo. I was taking 25mg not 50 dhea.

It seems like dhea and pregnenolone are the safest things. With testosterone and cortisol being the most dangerous to take. Although low dose cortisol seems ok.

But the interactions and what not are not things to mess with that's for sure :/

I'm glad you're ok now!

 

[CSMLSM]

Well it's definitely a steroid hormone. If you Google dhea and inflamation it comes up that dhea is a rather potent anti inflammatory. But I assume cortisol is the master anti inflammatory hormone.

Saying that I just meditated for ten minutes and thats also had an effect but not as good as the dhea of course.

I'd like to take 10mg hydrocortisone but I'm concernrd this will be immune suprressive. Although the UK drug website that doctor's use says that it's not at that dose. But I couldn't find another source to corroborate.

I feel better than I did thismorning. But I've had a busy isu day at work. I'm taking it easy.

But my tongue is very swollen and it hurts to talk a the moment. Typical ebv symptom. No doubt it's 100% ebv.

I've switched to 1g valtrex every 6 hours. 25mg dhea in the morning ideally and not at night. One andrographis dose in the am - which helped hugely but also brought on a slight temperature. Just praying I start to feel better. My body can't get sick until the weekend!

Stress is really screwing me over a the moment. I'm about to get a blood test for cortisol tomorrow. Be interesting to see what it shows.

Yes it is I made the comment about omega 3 because I use a cannabinoid (Caryophyllene) to activate SIRT1 and omega 3 is needed for cannabinoid receptors. Dhea activates lipid metabolism and affects immune cells because this affects PPAR`s through SIRT1.

 

[CSMLSM]

Here also-
Functional interactions between cannabinoids, omega-3 fatty acids, and peroxisome proliferator-activated receptors: Implications for mental health pharmacotherapies - PubMed (nih.gov)
Abstract
Cannabis contains a plethora of phytochemical constituents with diverse neurobiological effects. Cannabidiol (CBD) is the main non-psychotropic component found in cannabis that is capable of modulating mesocorticolimbic DA transmission and may possess therapeutic potential for several neuropsychiatric disorders. Emerging evidence also suggests that, similar to CBD, omega-3 polyunsaturated fatty acids may regulate DA transmission and possess therapeutic potential for similar neuropsychiatric disorders. Although progress has been made to elucidate the mechanisms underlying the therapeutic properties of CBD and omega-3s, it remains unclear through which receptor mechanisms they may produce their purported effects. Peroxisome proliferator-activated receptors are a group of nuclear transcription factors with multiple isoforms. PPARγ is an isoform activated by both CBD and omega-3, whereas the PPARα isoform is activated by omega-3. Interestingly, the activation of PPARγ and PPARα with selective agonists has been shown to decrease mesocorticolimbic DA activity and block neuropsychiatric symptoms similar to CBD and omega-3s, raising the possibility that CBD and omega-3s produce their effects through PPAR signaling. This review will examine the relationship between CBD, omega-3s, and PPARs and how they may be implicated in the modulation of mesocorticolimbic DAergic abnormalities and associated neuropsychiatric symptoms.

 

[CSMLSM]

Here also-
Emerging class of omega-3 fatty acid endocannabinoids & their derivatives - PubMed (nih.gov)
Abstract
Cannabinoid receptor activation is involved in homeostatic regulation of the body. These receptors are activated by cannabinoids, that include the active constituents of Cannabis sativa, as well as endocannabinoids (eCBs). The eCBs are endogenously synthesized from the omega-6 and omega-3 polyunsaturated fatty acids (PUFAs). The consumption of omega-3 fatty acids shifts the balance towards a higher proportion of omega-3 eCBs, whose physiological functions warrants further investigation. Herein, we review the discovery of omega-3 fatty acid derived eCBs that are generated from long chain omega-3 PUFAs - docosahexaenoyl ethanolamide (DHA-EA or synaptamide), docosahexanoyl-glycerol (DHG), eicosapentaenoyl ethanolamide (EPA-EA) and eicosapentanoylglycerol (EPG). Furthermore, we outline the lesser known omega-3 eCB-like molecules that arise from the conjugation of omega-3 fatty acids with neurotransmitters serotonin and dopamine - DHA-serotonin (DHA-5HT), DHA-dopamine (DHA-DA), EPA-serotonin (EPA-5HT) and EPA-dopamine (EPA-DA). Additionally, we describe the role of omega-3 eCBs and their derivatives in different disease states, such as pain, inflammation and cancer. Moreover, we detail the formation and potential physiological roles of the oxidative metabolites that arise from the metabolism of omega-3 eCBs by eicosanoid synthesizing enzymes - cyclooxygenase (COX), lipoxygenase (LOX) and cytochrome P450 epoxygenase (CYP450). In summary, we outline the novel findings regarding a growing class of signaling molecules that can control the physiological and pathophysiological processes in the body.

 

[godlovesatrier]

Interesting. Been taking omega 3 for 6 years. But the dhea is of course new. Took 25mg thismorning and that helped hugely with fatigue. It's about 11am now tho and I'm feeling a bit sickly. Although still recovering from ebv and my kidneys won't take anymore valtrex sadly so I am sort of stuck waiting for tenofovir to arrive.

Really glad I've stumbled across the dhea and its effects tho on inflamation. Hopefully there are no side effects. It's also made me feel calmer but a bit spaced out too. Not sure if it's made me feel "fogged" yet or if tbsrs the ebv effecting me.

 

[CSMLSM]

Interesting. Been taking omega 3 for 6 years. But the dhea is of course new. Took 25mg thismorning and that helped hugely with fatigue. It's about 11am now tho and I'm feeling a bit sickly. Although still recovering from ebv and my kidneys won't take anymore valtrex sadly so I am sort of stuck waiting for tenofovir to arrive.

Really glad I've stumbled across the dhea and its effects tho on inflamation. Hopefully there are no side effects. It's also made me feel calmer but a bit spaced out too. Not sure if it's made me feel "fogged" yet or if tbsrs the ebv effecting me.

Anyway I hope what you are trying works I was trying to answer your question

Advise welcome and ideas about the dhea making my fatigue better also v welcome. Never heard of anyone but Heaps getting anything from dhea.

The things it acts on are the same as the things I am using, just like LDN but obviously different things have better effect or need much lower/higher dosing. Omega 3 works on SIRT1 and PPAR`S, so does Dhea, LDN and Caryophyllene. I am almost symptom free and just need to perfect my dosing so I think Caryophyllene is great obviously

 

[godlovesatrier]

Yeah that's really very interesting.

Well the dhea is taking down the inflamation and the valtrex is going after the ebv.

I just got blood tests yesterday for a variety of issues including growth hormone (first time anyone's ever tested this!) But if my cortisol is completely flat I'll consider taking some small doses of hydrocortisone.

 

[CSMLSM]

I just got blood tests yesterday for a variety of issues including growth hormone (first time anyone's ever tested this!) But if my cortisol is completely flat I'll consider taking some small doses of hydrocortisone.

This is interesting and if you do not mind I would like to know the results of your growth hormone test.

If your cortisol is flat you may have adrenal fatigue and taking glucocorticoid receptor agonists beyond normal can blunt those receptors causing other issues resulting from natural biological feedback loops of processes to become dysfunctional and not work. This will mess with mood, circadian rhythm, sleep wake cycle among many others that rely on this feedback loop working properly. Look into sleep wake cycle and you will realise that one test in one day means nothing when testing for cortisol because of things like sleep wake cycle driven by cortisol level. Morning should be high so yes a low test should mean a better more indepth investigation and prolonged monitoring.

Let us know how you get on with it all.

 

[godlovesatrier]

I'm not sure what a high result is in units

I had a low cortisol test result 8.30am in January. Normally it's about 400 units. But no idea if that's correct or not. I've had 4 morning cortisol tests so that gives me a morning baseline.

Yesterday's was at 5pm so be interesting to see what that looks like.

Am aware of the issues around cortisol. Testing and treatment thereof. But good you mentioned it for others.

 

[godlovesatrier]

Should get test results tomorrow. Dhea not tested annoyingly

 

[CSMLSM]

Should get test results tomorrow. Dhea not tested annoyingly

Should be interesting to see the outcome and compare to what symptoms you are experiencing. Hopefully you can ascertain whats going on in your HPA axis and if you are adrenal fatigued or glucocoticoid receptor blunted which can happen because of adrenals overworking causing the atrophy (adrenals) and then receptors are blunted but with too little cortisol being produces so the whole system become surpressed and dysfunctional.

Sorry was just thinking and typing, like you said it might help someone.

 

[godlovesatrier]

Well a switch flipped yesterday and I'm now totally exhausted. Very weak. Muscles weak also. Dizzy. Lightheadded. Feels more like my cortisol production has gone sideways.

Still hesitant to take low dose hydrocortisone though due to covid.

My sleep has normalised and I could now sleep for 12 hours flat out. I do feel a bit better in the last third of that sleep cycle.

Definitely a hpa axis issue. Guess the dhea worked for a few days but once the inflammatory state had flipped. It was no longer of any benefit.

 

[godlovesatrier]

Felt great 24 hours ago. Like my normal self. But then took more dhea thinking that would be ok. That seemed to shut something down...if I had to guess. I can't be certain without the blood test results.

I have just chased the hospital for them as they aren't on my medical file. Probably because the hospital has them and they are not entwred into the gp system. It's so dumb how we have loads of separate systems here and most of them are from the 1960s.

A colleague worked on modernising them so I know how bad they are.

 

[godlovesatrier]

So I checked my cortisol morning blood tests. Cortisol in January showed a very low level half an hour after waking.

The rest of the time it showed about 400 which is normal I believe. So yeah seems like any stress even small amounts will cause the cortisol to tank. Hopefully my endocrinologist picks up on this.

 

[CSMLSM]

So I checked my cortisol morning blood tests. Cortisol in January showed a very low level half an hour after waking.

The rest of the time it showed about 400 which is normal I believe. So yeah seems like any stress even small amounts will cause the cortisol to tank. Hopefully my endocrinologist picks up on this.

Sounds like blunted glucocorticoid receptors could be the problem that have recovered slightly and become more sensitive from rest (not stressing, resting and pacing ect) and then have been overwhelmed with too much activation maybe (too high a dose maybe of meds). Just my thoughts on this puzzle but the earlier low low reading would fit with this.

I hope you figure out how best to address this with your endocrinologist. I wish I had had access to an endocrinologist, I have had to figure everything out on my own.