Quiet possibly our Adrenal is at fault

[Luckfax]

@spstriken

gefinauser
you are right.
how much is your Cortisol in blood? is it high or low? I see here many have higher or high normal. Mine is high normal too. I feel my symptoms are very much like cushing’s patient( big pot belly, thin legs, arms, little body hair etc)if you see pictures of dogs with cushings, they look like us. They do get pot belly and no body hair.click here
tinyurl.com/p8wrqyr

You do realise you’ve just linked to pictures of dogs?

All these so called signs of cushings certain posters keep referring to are symptoms of androgen deprivation. prostate-cancer.org/the-androgen … -syndrome/

[spstriken]

Luckfax
I am not saying Adeprivation may not the cause. we are look at mechanism, what organ has got damaged or the whole body. this study you posted does not rule in/out adrenal

[spstriken]

I mean to say after the damage has been done there is no point to discuss the cause.Now we need to investigate where damage has been done and what can be done to repair it now.

[gefinauser]

Never mind the discussion on the cause, I agree that we always should focus on the effect in fighting the symptons. If you can get through my big posts then you probably got what it takes to recover LOL.

@spstriken

gefinauser
you are right.
how much is your Cortisol in blood? is it high or low? I see here many have higher or high normal. Mine is high normal too. I feel my symptoms are very much like cushing’s patient( big pot belly, thin legs, arms, little body hair etc)if you see pictures of dogs with cushings, they look like us. They do get pot belly and no body hair.click here
tinyurl.com/p8wrqyr

Now my question is why many of us feel better on isocort despite high cortisol? Maybe external cortisol slows down our own body production? I am reading on curezone about this. People are saying isocort brings your own cortisol down.

Those in the known always says that taking blood cortisol is insufficient, due to different readings than what cortisol you got going on at the moment (this is just from the top of my head). From saliva is the accurate/correct way to go. The pattern should be always this: a spike in the moment you wake up (actually an hour before you wake up) and then slowly declining as the day goes on. Anything else at any time of the day and you got a problem.

I don’t know how many of us are actually using Isocort here in PH, I haven’t searched on that…
but my bet on the answer is on that “fatigue” side of things - supplying the substance the adrenals are made from relieves the stress placed on it. That’s at least how it feels for me when I take the pill, not that it’s what is technically actually going on. Since I don’t know if i’m actually supplying cortisol (at least in noticable amounts), I never take cortex on daily basis.

I do not have Cortisol tests on myself. Saliva tests costs about 350 euros in my country (a single one) and i’d have to pay that from my own pocket, plus I need a doctors prescription. No, I deducted with my own symptons. When I initially crashed, i kept losing all my energy to brainfog/crashed badly for roughly 11 hours - I read about adrenal gland problems so I stopped drinking green tea and coffee. Miraculously, the next day I was brainfog free/had most of my energies. However, days following that day I quickly fell into the constant brainfog problems you are familiar with.

2 years later, the pupil flashlight test came out (done by my doctor who knows this stuff as well) that I had slight dysfunction but my well-being after on adrenal cortex indicates that it goes way deeper/is much serious than the indications.

Now that I’m quite well recovered in adrenal’s (maybe 50% recovered), I actually had a day or two when drinking coffee actually gave me back my old self before finast, full mental clarity and power of imagination, the full monty - this, of course, followed by brainfog and listnessness as the adrenals got stressed from extra effort. Just saying this to show remarkable adrenals are.

The only way I can recover from adrenal stress so far is by

• ALWAYS relaxing - I don’t go to gym until I recover a bit more
• always working on that mental stress (damn, you would never think mental stress/worrying is physical but I have become a believer after working with my adrenal symptons for so long…),
• never sprinting or hurrying everywhere (i get adrenal-stressed and brainfogged for some hours after a sprint),
• avoiding coffee or other stimulants like chocolate,
• avoiding foods that cause stress to me like grains…
  Basically, it’s never anything that pushes or stimulates me more.

To put it simply: Any brainfog, apathy, anxiety, almost whatever i got going mentally - either affected by
*L-tyrosine (turns to… dopamine. Remember progesterone, dopamine results for us. Vitamin D is REQUIRED to make more dopamine… and dopamine plays a large part in everything.)
*or adrenal cortex
I have not tried progesterone or pregnelone yet and i don’t know if I will. I might recover without.

I use this product at times (not all the time! as that just gets you used to endogenous supply of cortisol, i suppose) iherb.com/Thorne-Research-Ad … =null&ic=1

–

That being said… spstriken, I know you got some balls and curious mind… If you are serious about recovering, maybe you should try treating this, especially if you got brainfod/apahty/no drive still? If you feel like it’s too much then just keep a lid on it and give it some time… some times take some L-tyrosine (powder form without anything else, order from Iherb or similiar) to get over brainfog and all those TRESSHOLD problems (you know, like “reading or understand this is too much” or “i just don’t have it in me to do this” or “it’s all too much” etc). Baby steps at a time.

Like i said in first post:
*Look into and buy Recovering with T3 from amazon. Find a doctor that will prescribe you with T3 (i think it’s best to go with this than Armour Thyroid). Try doing the Circadian Method, written in that book with that T3. Read more about adrenal problems from Stop the Thyroid Madness or from -JN-'s topic. When you get fogged, supply with either L-tyrosine or adrenal cortex.
*Other route is to try methylation protocol here in the theories section. tl;dr: methylation problems have a lot to do with hypothyroidism, hypot = adrenal problems as well, we got a strong history with methylation problems so far (whoever here got their methylation panel analyzed).

If you start these steps then you probably got the determination to see your recovery through… I know you can do it.

I think I’ve said everything. I got even more interesting experiences I can’t recall from the top of my mind but i’m pretty sure they are all just to demonstrate the importance of adrenals - treating adrenals is equally important step when treating hypothyroidism as well. Anything more is maybe unnecessary, I’m only motivated by trying to get people help themselves and this is already pushing it a lot (since i can’t know how many people here actually try to actively recover themselves). I’m starting to understand the people who avoid the forum for the sake of focusing on their newfound determination or their recovered life. wish you the best on your road to recovery.

[spstriken]

thanks for your time and advice.

[spstriken]

@Enden

The adrenal glands are definitely involved. I recently checked cortisol in saliva, and it was 6 nmol/l 09.00 AM (range 3.5 - 27 nmol/l) and 6 nmol/l 11.00 PM (range <6 nmol/l). What’s interesting here, besides that the free cortisol level was low in the morning and high in the evening, is that it didn’t have a circadian rhythm. Also, I’ve experimented with dexamethasone for a week, and woke up with a morning erection most of the days… It caused symptoms of gynecomastia to subside too, so I’m sure that the adrenal glands are responsible for elevated levels of estrogens. The latest PFS study showed that pregnenolone and estradiol were significantly elevated in PFS subjects. Considering that negative feedback is controlled by cortisol, it’s likely that free cortisol deficiency is involved.

Effects of finasteride, a 5 alpha-reductase inhibitor, on circulating androgens and gonadotropin secretion in hirsute women.

Abstract
An oral 5-mg dose of finasteride, a 5 alpha-reductase inhibitor, was administered for 3 months to 10 hirsute women to determine the effect on gonadotropin secretion, on basal and stimulated androgen secretion, and on hair growth. Hair growth was assessed by the Ferriman-Gallwey score. All of the above determinations were evaluated before and after 1 and/or 3 months of finasteride treatment. Basal and GnRH-stimulated gonadotropin secretions were not affected. Indeed, finasteride did not modify the pulsatility of LH secretion. No change was seen in estradiol, PRL, free testosterone, androstenedione, dehydroepiandrosterone sulfate, and sex hormone-binding globulin concentrations. Serum concentrations of cortisol (F) were significantly reduced after 1 month of finasteride treatment. The F levels returned to pretreatment levels after 3 months. Plasma levels of dihydrotestosterone and 3 alpha-androstanediol glucuronide significantly decreased during finasteride treatment. A significant increase in testosterone concentrations was observed after 3 months. Finasteride did not modify the responses of testosterone, androstenedione, and dehydroepiandrosterone sulfate to ACTH-(1-24) injection. Conversely, finasteride blunted the F response to corticotropin stimulation. Three months of finasteride treatment significantly decreased the Ferriman-Gallwey score. In conclusion, finasteride significantly decreased dihydrotestosterone and hair growth in hirsute women without negatively affecting gonadotropin secretion.

press.endocrine.org/doi/abs/10.1 … .3.8077369

5α-reductase is a regulator of glucocorticoid action and metabolic phenotype in human liver

Patients with GC excess (Cushing’s syndrome) develop central obesity, insulin resistance and hepatic steatosis. The A-ring reductases (5α-reductase type 1 (5αR1) and 2 (5αR2)) generate dihydrotestosterone from testosterone, but importantly also inactivate cortisol and are highly expressed in human liver. We propose that 5αR may regulate GC exposure and therefore may modulate metabolic phenotype in human liver.

Primary human hepatocytes and the C3A human hepatoma cell line were incubated with cortisol (0–1000 nM), alone or in combination with the selective 5αR2 inhibitor, Finasteride (500 nM) or non-selective inhibitor, Dutasteride (500 nM) for 24 h. In addition, C3A cells (which express 5αR1, but not 5αR2), were transfected with a plasmid containing either WT, or inactivated mutant (R246Q) 5αR2. The functional impact of these manipulations was assessed through real-time PCR based gene expression, enzyme activity assays using both gas and liquid chromatography/mass spectrometry and functional assessments of de novo lipogenesis (DNL).

Cortisol decreased DNL in a dose-dependent manner (e.g. 85.66.6% (100 nM), 73.57.9% (250 nM), 55.045.6% (1000 nM), P<0.05). 5αR2 over-expression increased DHT generation and cortisol clearance and in the absence of cortisol, did not alter rates of DNL. However, in the presence of cortisol, 5αR2 restored DNL to levels observed in untreated controls (e.g. 61.9±7.6% (cortisol) vs 103.8±8.8% (5αR2+cortisol), P<0.05, control=100%). Complementary experiments using the R246Q 5αR2 construct did not alter cortisol-mediated suppression of DNL. Furthermore, both Finasteride and Dutasteride augmented the action of cortisol to supress DNL in primary cultures of human hepatocytes (e.g. 88.3±5.3 vs 76.9±5.2%, cortisol vs cortisol+finasteride, P=0.05).

We have demonstrated that manipulation of 5αR activity can regulate metabolic phenotype in human liver. Further clinical studies are now warranted, but this may have significant clinical implications for those patients with mutations in 5αR2 and those prescribed 5αR inhibitors.

endocrine-abstracts.org/ea/0 … 4oc3.2.htm

Finally, glucocorticoid availability can be influenced by manipulation of steroid breakdown. For example, non-selective (dutasteride) and type 2 selective (finasteride) 5α-reductase inhibitors (Figure 1B), which are used in the treatment of benign prostatic hyperplasia and male pattern baldness (Metcalf et al., 1989), may also inhibit metabolic clearance of glucocorticoids.

ncbi.nlm.nih.gov/pmc/article … po=13.2653

it looks like your cortisol remains the same 24 hours.is it maybe due poor metabolism of Cortisol? just like for some fre T is low but total T is high?

[spstriken]

@Enden

The adrenal glands are definitely involved. I recently checked cortisol in saliva, and it was 6 nmol/l 09.00 AM (range 3.5 - 27 nmol/l) and 6 nmol/l 11.00 PM (range <6 nmol/l). What’s interesting here, besides that the free cortisol level was low in the morning and high in the evening, is that it didn’t have a circadian rhythm. Also, I’ve experimented with dexamethasone for a week, and woke up with a morning erection most of the days… It caused symptoms of gynecomastia to subside too, so I’m sure that the adrenal glands are responsible for elevated levels of estrogens. The latest PFS study showed that pregnenolone and estradiol were significantly elevated in PFS subjects. Considering that negative feedback is controlled by cortisol, it’s likely that free cortisol deficiency is involved.

Effects of finasteride, a 5 alpha-reductase inhibitor, on circulating androgens and gonadotropin secretion in hirsute women.

Abstract
An oral 5-mg dose of finasteride, a 5 alpha-reductase inhibitor, was administered for 3 months to 10 hirsute women to determine the effect on gonadotropin secretion, on basal and stimulated androgen secretion, and on hair growth. Hair growth was assessed by the Ferriman-Gallwey score. All of the above determinations were evaluated before and after 1 and/or 3 months of finasteride treatment. Basal and GnRH-stimulated gonadotropin secretions were not affected. Indeed, finasteride did not modify the pulsatility of LH secretion. No change was seen in estradiol, PRL, free testosterone, androstenedione, dehydroepiandrosterone sulfate, and sex hormone-binding globulin concentrations. Serum concentrations of cortisol (F) were significantly reduced after 1 month of finasteride treatment. The F levels returned to pretreatment levels after 3 months. Plasma levels of dihydrotestosterone and 3 alpha-androstanediol glucuronide significantly decreased during finasteride treatment. A significant increase in testosterone concentrations was observed after 3 months. Finasteride did not modify the responses of testosterone, androstenedione, and dehydroepiandrosterone sulfate to ACTH-(1-24) injection. Conversely, finasteride blunted the F response to corticotropin stimulation. Three months of finasteride treatment significantly decreased the Ferriman-Gallwey score. In conclusion, finasteride significantly decreased dihydrotestosterone and hair growth in hirsute women without negatively affecting gonadotropin secretion.

press.endocrine.org/doi/abs/10.1 … .3.8077369

5α-reductase is a regulator of glucocorticoid action and metabolic phenotype in human liver

Patients with GC excess (Cushing’s syndrome) develop central obesity, insulin resistance and hepatic steatosis. The A-ring reductases (5α-reductase type 1 (5αR1) and 2 (5αR2)) generate dihydrotestosterone from testosterone, but importantly also inactivate cortisol and are highly expressed in human liver. We propose that 5αR may regulate GC exposure and therefore may modulate metabolic phenotype in human liver.

Primary human hepatocytes and the C3A human hepatoma cell line were incubated with cortisol (0–1000 nM), alone or in combination with the selective 5αR2 inhibitor, Finasteride (500 nM) or non-selective inhibitor, Dutasteride (500 nM) for 24 h. In addition, C3A cells (which express 5αR1, but not 5αR2), were transfected with a plasmid containing either WT, or inactivated mutant (R246Q) 5αR2. The functional impact of these manipulations was assessed through real-time PCR based gene expression, enzyme activity assays using both gas and liquid chromatography/mass spectrometry and functional assessments of de novo lipogenesis (DNL).

Cortisol decreased DNL in a dose-dependent manner (e.g. 85.66.6% (100 nM), 73.57.9% (250 nM), 55.045.6% (1000 nM), P<0.05). 5αR2 over-expression increased DHT generation and cortisol clearance and in the absence of cortisol, did not alter rates of DNL. However, in the presence of cortisol, 5αR2 restored DNL to levels observed in untreated controls (e.g. 61.9±7.6% (cortisol) vs 103.8±8.8% (5αR2+cortisol), P<0.05, control=100%). Complementary experiments using the R246Q 5αR2 construct did not alter cortisol-mediated suppression of DNL. Furthermore, both Finasteride and Dutasteride augmented the action of cortisol to supress DNL in primary cultures of human hepatocytes (e.g. 88.3±5.3 vs 76.9±5.2%, cortisol vs cortisol+finasteride, P=0.05).

We have demonstrated that manipulation of 5αR activity can regulate metabolic phenotype in human liver. Further clinical studies are now warranted, but this may have significant clinical implications for those patients with mutations in 5αR2 and those prescribed 5αR inhibitors.

endocrine-abstracts.org/ea/0 … 4oc3.2.htm

Finally, glucocorticoid availability can be influenced by manipulation of steroid breakdown. For example, non-selective (dutasteride) and type 2 selective (finasteride) 5α-reductase inhibitors (Figure 1B), which are used in the treatment of benign prostatic hyperplasia and male pattern baldness (Metcalf et al., 1989), may also inhibit metabolic clearance of glucocorticoids.

ncbi.nlm.nih.gov/pmc/article … po=13.2653

it looks like your cortisol remains the same 24 hours.is it maybe due poor metabolism of Cortisol? just like for some fre T is low but total T is high?
My blood cortisol is always high, don’t know about salivary level yet.

[Enden]

I don’t know. I think that free cortisol is too low, and that the brain only makes the problem worse by attempting to increase cortisol, due to a negative ratio between adrenal androgens and cortisol. The androgens aromtatizes, and it leads to more CBG, which probably means less free cortisol, or unchanged at best. Since aromatase inhibitors only gives us temporary relief, it’s likely that this is a consequence. After all, finasteride has been shown to blunt the cortisol response to ACTH - and that’s probably the root cause.

Anyway, something is definitely wrong when the cortisol level doesn’t have a circadian rhythm, and I’m going to get to the bottom of this. Interestingly, several people have reported a 17-OH-Progesterone level above the normal range, which indicates non-classic CAH due to 21-hydroxylase deficiency. We may have had a slight deficiency (non-symptomatic), that finasteride changed into a real problem, by interfering with the amount of free cortisol through elevation of estradiol.

[Enden]

I need to add that my serum cortisol has been mid- to high range. I haven’t checked free cortisol before now.

[Raberduck]

I ordered a cortisol saliva test (3 samples: morning, noon, evening) and will post my results here. I’m really curious!! Last year I had mid cortisol levels in blood (morning).

[spstriken]

some people have reported that when they took ACTH they felt bad after and when took Dexamethasone they felt better. this all point towards cortisol issues.

[spstriken]

Undetectable urinary free cortisol concentrations in a case of
Cushing’s disease

eje-online.org/content/140/2/148.full.pdf

[Enden]

@spstriken

some people have reported that when they took ACTH they felt bad after and when took Dexamethasone they felt better. this all point towards cortisol issues.

There’s definitely an issue with cortisol.

[Enden]

@Raberduck

I ordered a cortisol saliva test (3 samples: morning, noon, evening) and will post my results here. I’m really curious!! Last year I had mid cortisol levels in blood (morning).

Great! I can’t wait.

[Jonson]

i also felt a lot worse with hydrocortisone and things that realted to it.
i want to try dexamethason and see what happen

[spstriken]

eje-online.org/content/140/2/148.full.pdf
Note from above case, similarities with us
‘moon face’, central adiposity and slight proximal muscle weakness. There was no
evidence of a ‘buffalo hump’, supraclavicular fat pads,
ecchymosis, abdominal striae or hirsutism. She had
noticed a change in her facial appearance and easy
bruising over the past 3 years

Alsol notice
failure of cortisol suppression
with low-dose (0.5 mg 6 hourly for 48 h), but not
high-dose (2 mg 6 hourly for 48 h) dexamethasone.

I don’t say that we have 100% cushing’s but this is something very similar to cushing’s. Adrenal or kidneys has some role here.

[spstriken]

looks like even Mew once thinking in the same line and I don’t know what happened then.
Please look at the blood report here of Terp03. pay atention to hormones which are mentioned in the paper at the start of this thread especially
Cortisol high
Androstenedione high

viewtopic.php?f=4&t=1218&hilit=urinary+free+cortisol

I am surprised on this forum I don’t see any 24hr urine cortisol test. Few weeks back I requested my dr for 24 hr urine cortisol but he declined, I don’t know why, the money was not going out of his pocket. I will try soon with another dr.

[Livingdead]

Anyone tried the Natural desiccated thyroid they mention on the Stop the Thyroid Madness website?

[spstriken]

@Livingdead

Anyone tried the Natural desiccated thyroid they mention on the Stop the Thyroid Madness website?

first treat adrenal then thyroid.

[Livingdead]

I was checking where it was in the body and was surprised to see it’s right where I have a pain that comes and go on my left. I began to have that pain about a year and a half before my crash. I actually had a gradual degradation of sleep and of my capacity to sustain stress starting around that time and had the crash when I stopped the pill (I started again later thinking it couldn’t be that because I wasn’t taking it anymore and was getting worse and worse). Anyway, I got an ultrasound examination for the pain, but they didn’t find anything. I know it’s something that has to do with fin side effects because it coincides with the beginning of other sides that, I know now, were caused by the drug.

I’m going to do some research on the matter, and maybe read the thread again from the start.