Hormones And Hairloss

[tallglass13]

Pregnenolone + biotin helps synthesize cortisol... cortisol is anti-inflammatory... and if we're constantly inflamed we would be using up all of our cortisol stores... Make sense that we would have to replenish those stores, just as we would have to replenish our B vitamins, glycogen or anything else that gets used a lot

 

[gilson d dantas]

Oh yes I think you have posted this before somewhere. That was an interesting response from Ray, he is usually very humble in his speech and emails but I suppose this struck a bad chord with him.

Like I said before, I believe that cortisol and thyroid are mutually exclusive, to say they are working together seems silly. I would like to know where he drew these ideas from, what studies he was looking into, what scientists he was reading. Thyroid delivers many important functions but when it is not available cortisol and other stress hormones step in, and carry out similar functions but do significant damage and degeneration to the system. There are plenty of studies to support this, that cortisol is inflammatory and contributes to disease.

I wonder if this guy is still around maybe he can show us his work. If cortisol does have unique physiological benefits above and beyond thyroid, then it would function as a double edged sword, and i would certainly like to understand that more.

You are completely right! Raincoast´s perspective is wrong: cortisol and thyroid are mutually exclusive...

 

[Lokzo]

This would make sense why Adrenal Cortex does me wonders. I have extremely low cortisol production, and I find it really does help me with energy/mood.

 

[Lokzo]

I also honestly feel like homeopathy has potential to boost cortisol levels. You just need to know how to REPORTORIZE.

 

[ddjd]

This would make sense why Adrenal Cortex does me wonders. I have extremely low cortisol production, and I find it really does help me with energy/mood.

Out of interest, if you take it before bed does it help you sleep or wake you up? I find it sends me to sleep and I sleep so well. Does that mean I've got low Cortisol do you think??

I'm taking seeking health Adrenal cortex 50mg

Apparantly there's a difference between taking adrenal cortex v Adrenal glandular

 

[Lucas]

This would make sense why Adrenal Cortex does me wonders. I have extremely low cortisol production, and I find it really does help me with energy/mood.

What brand of Adrenal Cortex?

 

[Frankdee20]

The thing is that Ray takes pregnenolone and is a big proponent of pregnenolone, but it seems that pregnenolone boosts the cortisol to good levels.. and when those levels are filled then it could boost progesterone just as Ray says it does. I had to read the thread over and over and over again to really get the gist of what he is saying
So Mr. Peat has been boosting his cortisol production along with taking his thyroid

I thought Pregnenalone was the most potent inhibitor of CRH, and thus lower Cortisol ? Maybe Progesterone then converts to Cortisol. That is why Preg needs to be taken with food.

 

[Kartoffel]

I thought Pregnenalone was the most potent inhibitor of CRH, and thus lower Cortisol ? Maybe Progesterone then converts to Cortisol. That is why Preg needs to be taken with food.

Of course progesterone converts to cortisol, but increasing pregnenolone doesn't upregulate this process. It's not like a cascade where all the basins downstream will overflow, if you pour in more water at the top. Even taking 500mg for several weeks will not increase cortisol, but actually slightly lower it.

Proof-of-Concept Trial with the Neurosteroid Pregnenolone Targeting Cognitive and Negative Symptoms in Schizophrenia

 

[Lokzo]

What brand of Adrenal Cortex?

Thourne.

 

[CDT]

This is one of the finds that led me to Ray Peat years ago.
Thoughts anyone?





THE DETAILED CAUSES OF MALE PATTERN BALDNESS AND PROSTATE GROWTH

Overview:

when systemic progesterone and systemic cortisol levels are too low, this causes too high DHT metabolism in hair follicles which in turn causes excess free radical damage to the hair follicles on our head in areas where the blood flow is restricted (“due to genetic predisposition”). The additional lack of blood flow to hair follicles means the free radical damage to hair follicles cannot be repaired adequately.

The same excess-free-radical-damage-due-to-excess-DHT-metabolism occurs in our prostate, inflaming our prostate causing either pain and / or constricting the urethra thus reducing urine flow.

This overview omits a lot of important details, so you MUST also read the following detailed explanation before discounting the above info.

Details:

Relatively high levels of progesterone are necessary to compete with DHT for DHT receptors. When progesterone triggers a DHT receptor, then DHT cannot trigger that receptor, and the progesterone which enters the cell triggers progesterone’s actions not DHT’s actions.

Relatively high levels of progesterone are necessary to up-regulate the p53 tumour suppressor protein, which is postulated as one of the primary means of minimizing prostate tumors.

Relatively high levels of cortisol are necessary to oppose / downregulate DHT metabolism. Cortisol acts directly on our genes to limit the ability of T and DHT to trigger their own genetic effects.

When the cortisol-production-line hormones progesterone and cortisol are too downregulated, then cells will aromatase T into E2, and use the E2 to oppose T metabolism and DHT metabolism. To our cells, this is “Plan B”. “Plan A” is to use progesterone and cortisol to oppose / downregulate T and DHT metabolism.

While using E2 to oppose T metabolism and DHT metabolism works well in cells which absorb DHT from serum, it works very poorly in cells which manufacture their own DHT (eg: prostate, and hair follicles, ie: all cells with plenty of 5α reductase). Hence these cells continue to experience too high DHT metabolism even in the presence of too high E2.

At the onset of male pattern baldness, our progesterone and our cortisol have gone too low, which would allow T metabolism and DHT metabolism to go too high, so our cells invoke their secondary defence mechanism and increase E2, and they then use E2 to oppose T metabolism and DHT metabolism.

When progesterone is relatively too low, this spells that all of the cortisol-production-line hormones (eg: preg, prog, cortisol) are downregulated to below optimum, and this is why the solution is to restore the optimal hormone levels in the cortisol-production-line.

HALTING AND POSSIBLY REVERSING MALE PATTERN BALDNESS
Addressing The Root Cause

Addressing the root cause requires boosting systemic progesterone (not necessarily by supplementation with progesterone) and boosting systemic cortisol (not necessarily by supplementing with HC, which is man made bioidentical cortisol), up to the level which balances systemic DHT metabolism.

Unfortunately for most males, boosting the cortisol-production-line also requires boosting thyroid hormones T3 and T4, because once the cortisol-production-line hormones are lowered, our cells automatically downregulate our T3 to match our reduced cortisol levels, which creates an excess of T4 (T3 is made from T4). When our hypothalamus detects excess T4, it downregulates the synthesis of T4 in the thyroid gland.

Unfortunately once our hypothalamus downregulates our T4, our body enters a very stable state with a reduced resting metabolic rate. When this occurs, boosting the cortisol-production-line hormones requires boosting our resting metabolic rate, and that requires a three phased solution approach, ie:

Phase 1: Restore preg, prog and cortisol, via supplementary transdermal pregnenolone (or prog), to as good as can be achieved without thyroid hormones.

Phase 2: Restore thyroid hormones, pref via supplementary slow-release-compounded T3 (not yet T4) and adjust both preg and T3 thyroid hormones together to achieve optimum balance as well as optimum levels of all cortisol-production-line hormones as well as optimum levels of thyroid hormones.

Phase 3: Swap out as much T3 with T4 as possible (definitely possible) and swap out as much pregnenolone with dietary cholesterol as possible (less effective with increasing age).

This is explained in Hormone Modulation Therapy 101 (HMT101) scroll down to “What process should my doctor follow…”, and the details re pregnenolone supplementation are explained in Cortisol Boost 101 (CB101), scroll down to “Finding the pregnenolone and progesterone “top up” sweet spots”. The details re thyroid hormone supplementation are explained in Thyroid Boost 101 (TB101), scroll down to “Dosing suggestions for T3-only, and T4-only”.

HALTING AND POSSIBLY REVERSING MALE PATTERN BALDNESS
Leaving The Root Cause In Place By Reducing Hair Follicle DHT Metabolism

Option 1: Infra Red or Laser Thermal Treatment of Hair Follicles.

This increases the metabolic rate of the hair follicle cells, so they absorb more hormones including progesterone, and they allow the free radical damage to be repaired.

Option 2: Localized DHT Metabolism Reduction: Hair Follicles Only

Only Big Pharma drugs are available to achieve this, and the best of these are topical low concentration ketoconazole (eg: Nizoral) and spironolactone (eg: Aldactone)

Provided you keep the concentration low, then these do have mild systemic effects, however in many cases a small degree of systemic DHT suppression is required to help keep DHT metabolism in the prostate in check, and some people have discovered that ceasing their ketoconazole and / or spironolactone treatment results in mild prostate inflammation.

Option 3: Systemic Reduction Of DHT Metabolism: Only Use This If Systemic DHT Metabolism Is High

WARNINGS:
1) A little suppression of systemic DHT metabolism may reduce libido.
2) Too much suppression of systemic DHT metabolism will definitely reduce libido.
3) If your cortisol-production-line is too downregulated while you’re undergoing systemic DHT suppression therapy, then this can “tip you over the edge” and strongly suppress your entire cortisol-production-line (the “finasteride effect”). This can happen after a week if your cortisol-production-line is too downregulated when you start systemic DHT suppression therapy, or it can occur after several years as aging will eventually downregulate your cortisol-production-line hormones over time.

How to measure systemic DHT metabolism is explained here (hint: 24 hr urinalysis of several specific metabolites is necessary):
http://musclechatroom.com/forum/show…36&postcount=4

The Big Pharma drugs available to specifically reduce DHT metabolism, without directly reacting with other hormones, are dutasteride (eg: Avodart) and finasteride (eg: Proscar, Propecia)

The natural substance isolates / extracts which specifically reduce DHT metabolism are saw palmetto (not sure if there are any others).

Of these three substances, low dose dutasteride (eg: Avodart) is able to be managed much more reliably than both finasteride and saw palmetto (more on this below), and when finasteride or saw palmetto are not managed adequately in some people, those people have experienced a severe crash of the cortisol-production-line hormones – and these people have formed self-help groups such as propeciahelp.com, mypropeciasideeffects.com, etc…

NB: all these people need to do is restore their cortisol-production-line hormones to optimum, but:
a) they don’t understand what their cortisol-production-line hormones are,
b) they’re prepared to undergo “quick fix” hormone modulation therapy using finasteride or saw palmetto, but they’re usually not prepared to undergo the much slower but much more reliable process of boosting their cortisol-production-line hormones.

HALTING AND POSSIBLY REVERSING MALE PATTERN BALDNESS
Recovering Libido

The only option to maintain hair and recover libido is to boost the cortisol-production-line hormones (eg: preg, prog, cortisol) as much as possible, and in addition boost thyroid hormones T4 and T3 up to the limit imposed by the maximum cortisol levels.

Determining the max boost to the cortisol-production-line hormones and thyroid hormones as an iterative process (boost preg/prog/cortiso, then boost T4/T3, boost preg/prog/cortisol a little more, boost T4/T3 a little more, etc…) This will boost overall metabolism, which includes boosting systemic T and systemic DHT, yet the DHT metabolism boost within hair follicles and the prostate is kept manageable, ie: there is no excessive free radical damage to these tissues so hair follicles stay healthy and the prostate remains normal size.

WHAT SPECIFICALLY ABOUT FINASTERIDE AND SAW PALMETTO CAUSES THIS HORMONE CRASH ?

While finasteride (eg: Proscar, Propecia) lowers systemic DHT metabolism similar to dutasteride, the fact that the half life of finasteride is anywhere from 4 hours (in fast metabolizers) to as high as 12 hours (in slow metabolizers), which means the effective life of the finasteride or saw palmetto can be anywhere from 6 hours to 18 hours. This means that the amount of suppression / downregulation of DHT metabolism can be much greater than anticipated.

The problem with excessive DHT suppression / downregulation is that DHT triggers many of the same gene expression actions as T (not 100% overlap) and therefore suppression / downregulation of DHT results in downregulation of our testosterone metabolism.

Since one of progesterone’s and cortisol’s critical functions is to oppose T and DHT metabolism, therefore when T and DHT metabolism activity declines (includes genetic expression effects), then cells downregulate their cortisol and progesterone receptors and absorb less cortisol and less progesterone. This is because they need less “opposition” or “downregulation” of T and DHT.

The way the body achieves this negative feedback loop is by downregulating the entire cortisol-production-line (eg: preg, prog, cortisol). But once the cortisol-production-line hormones are lowered, our cells automatically downregulate our T3 to match our reduced cortisol levels, which creates an excess of T4 (T3 is made from T4). When our hypothalamus detects excess T4, it downregulates the synthesis of T4 in the thyroid gland.

Unfortunately once our hypothalamus downregulates our T4, our body enters a very stable state with a reduced resting metabolic rate. Once we’ve entered this very stable state with a lowered resting metabolic rate, most males who then back out their finasteride or saw palmetto can only recover their previous hormone levels (along with their previous high resting metabolic rate) very very slowly, and some will never recover their previous high hormone levels without intervention.

Once we’ve entered this very stable state with a lowered resting metabolic rate, the intervention required is to boost the cortisol-production-line hormones by boosting resting metabolic rate, and that requires the three phased solution approach, explained in the previous section “Addressing the root cause”.

HOW DO I PREVENT MY HORMONES CRASHING WHEN SUPPRESSING DHT ?

While it’s simple to explain at a high level, it’s a complex process when implemented: You need to initially monitor your sex hormones and your cortisol-production-line hormones (eg: preg, prog, cortisol) and if these are too low initially then you will need to either abstain from using DHT suppressants / downregulators, or you must first optimize at least your cortisol-production-line hormones (eg: preg, prog, cortisol) until your E2 is lowered, before commencing to suppress DHT.

This process is described in the Cortisol boost 101 primer, and you can access that from the links in the Hormones 101 primer, which is a sticky on the front page of this AllThingsMale forum.

WHAT IF INCREASED SERUM PROGESTERONE DOESN’T REVERSE MALE PATTERN BALDNESS ?

That’s usually because the progesterone isn’t being absorbed by cells, which is usually because those cells have an overall metabolic rate which is too low.

Since the progesterone is synthesizing into some cortisol (just not enough) the reason for the too low metabolic rate in these cells is not due to inadequate cortisol. In this case it’s due to inadequate thyroid hormone T4.

Once T4 levels are restored to optimum, the cells will absorb both the T4 (which gets synthesized into T3) and extra cortisol, and they will boost their overall metabolic rate to optimum, and that’s when they’ll start absorbing more progesterone.

WHY IS THE DHT METABOLISM IN MY HAIR FOLLICLES HIGH, YET I DON’T HAVE EXCESSIVE LIBIDO, AND / OR MY ERECTION PERFORMANCE IS BELOW PAR ?

Since libido and erection performance are promoted by DHT which originates from cells which absorb DHT from serum (ie: not the prostate, not hair follicles), and since these cells are using relatively high E2 to oppose / downregulate their DHT metabolism, therefore the cells which promote libido and erection performance are doing a poor job of triggering adequate libido, and they’re doing a poor job of triggering adequate erection performance.

When these cells use increased levels of progesterone and cortisol to oppose / downregulate T metabolism and DHT metabolism, then IF your thyroid hormone T4 levels rise to match the increase in your cortisol (more likely in younger males, less likely in older males), then your overall metabolic rate will increase, and this includes your systemic T and DHT metabolism but NOT your hair follicle or your prostate DHT metabolism ! Thus your libido and erection performance will remain unchanged, yet your hair will stay put, and your prostate will shrink to normal size.

HOWEVER (WARNING!) When these cells use increased levels of progesterone and cortisol to oppose / downregulate T metabolism and DHT metabolism, then IF your thyroid hormone T4 levels do not rise to match the increase in your cortisol (more likely in older males, less likely in younger males), then your overall metabolic rate will not increase, so your systemic T and DHT metabolism will not increase. Thus your libido and erection performance will decrease. In this case you must boost your thyroid hormones too. This is explained in the Thyroid boost 101 primer, which has a link in the Hormones 101 “sticky” on the first page of this AllThingsMale subforum.

PAPERS / REFERENCES

1) Confirmation of ability of progesterone to inhibit DHT in hair follicles:

Journal: European Journal of Dermatology. Volume 11, Number 3, 195-8, May – June 2001, Revues
Title: “Influence of estrogens on the androgen metabolism in different subunits of human hair follicles”
URL full text

2) Confirmation of cortisol’s ability to downregulate T

Journal: JCEM
Title: Acute Suppression of Circulating Testosterone Levels by Cortisol in Men
URL abstract

and

Journal: Journal of Molecular Endocrinology, 41, 165-175.
Title: Glucocorticoids antagonize cAMP-induced Star transcription in Leydig cells through the orphan nuclear receptor NR4A1
URL full text

3A) Confirmation that hair follicles which have their own 5α reductase absorb serum T to manufacture most of their own DHT.

Journal: Archives of Dermatological Research. 1998 Mar;290(3):126-32.
Title: 5 alpha-reductase activity in the human hair follicle concentrates in the dermal papilla.
URL abstract

3B) Corollary: Since increasing cortisol downregulates T synthesis, therefore increasing cortisol also downregulates the synthesis of DHT within hair follicle cells.

That’s because hair follicle cells don’t absorb much DHT directly, but instead they absorb T from serum and synthesize that into DHT via the action of 5α reductase.

4A) Confirmation that upregulation of serum DHT levels follows upregulation of hair follicle DHT levels (not to the same extent):

I don’t have an obvious demonstration of this.

4B) Confirmation that downregulation of serum DHT levels follows downregulation of hair follicle DHT levels (not to the same extent):

Journal: Journal of the American Academy of Dermatology Volume 55, Issue 6 , Pages 1014-1023, December 2006
Title: The importance of dual 5α-reductase inhibition in the treatment of male pattern hair loss: Results of a randomized placebo-controlled study of dutasteride versus finasteride
URL abstract
URL detailed summary

4C) Assumption with high likelihood of being correct: Since the downregulation of serum DHT levels follows downregulation of hair follicle DHT levels (but not to the the same extent), that the upregulation of serum DHT levels follows downregulation of hair follicle DHT levels (but not to the the same extent).

While you might choose to be pedantic and dispute this assumption, if you rejected the hard fact that both progesterone and cortisol downregulate DHT in hair follicles, just because you chose to dispute this assumption, then you’d be throwing the baby out with the bathwater.

5A) Confirmation that E2 does not suppress DHT metabolism adequately in cells which manufacture their own DHT

[TO DO]

ACCURATE MONITORING OF DHT METABOLISM

Unfortunately serum DHT levels get high when DHT gets “backed up” and DHT is not being used up (ie: when DHT metabolism is low). This is quite unlike testosterone, which does not get “backed up” when T is not being used.

When DHT is being used up, more DHT needs to be synthesized, ie:
testosterone —5α reductase—> DHT

Therefore any biomarker which can indicate the activity of 5α reductase enzymes also indicates the rate of synthesis of DHT from testosterone, and thus indicates DHT metabolism.

Via experimental research, several research teams have confirmed that the synthesis of tetrahydrocortisol —5α reductase—> 5α tetrahydrocortisol (5αTHF)

…can be monitored using 24hr urinary analysis, and the ratio of 5αTHF to THF follows the 5α reductase activity, ie:

high ( 5αTHF / THF ) shows high 5α reductase activity
low ( 5αTHF / THF ) shows low 5α reductase activity

Taken together, these are good indicators of 5α reductase activity, and thus DHT metabolism. Dr Crisler seems to agree.

The following research teams confirmed that the ratio of 5αTHF to THF follows the 5α reductase activity, and thus DHT metabolic activity, eg:

Title: Diagnosis of 5alpha-reductase 2 deficiency: a local experience
Journal:
Author(s):
URL Full Text

NB: 5a THF/THF normal ratio range is between 0.5 and 2.5 quoted in “Diagnosis of 5alpha-reductase 2 deficiency: a local experience”.

Title: The Diagnosis of 5{alpha}-Reductase Deficiency in Infancy
Journal: blah
Author(s): blah
URL Full Text

Title: A Case of 5 alpha-reductase Deficiency in Infancy
Journal: blah
Author(s): blah
URL Full Text

Title: Early diagnosis and management of 5 alpha-reductase deficiency
Journal: blah
Author(s): blah
URL Full Text

Title: Increased 5{alpha}-Reductase Activity and Adrenocortical Drive in Women with Polycystic Ovary Syndrome
Journal: blah
Author(s): blah
URL Full Text

Would it be safe to take saw palmetto as a supplement in any case? Or should we avoid it until we have information. I would imageine that Saw palmetto would be milder than drugs with more significant effects on DHT metabolism...

 

[Lokzo]

Would it be safe to take saw palmetto as a supplement in any case? Or should we avoid it until we have information. I would imageine that Saw palmetto would be milder than drugs with more significant effects on DHT metabolism...

I never noticed any negatives from Saw Palmetto, and I was using pretty high doses.

 

[boxers]

Informative

 

[lampofred]

Why did Dr. Peat react so negatively to the post? Does anyone still have his reply? I thought it was far more accurate than the typical excess testosterone theory for hair loss. Now that I think about it, raising cortisol very high (via caffeine) was what cured my hair loss. I do remember reading that first post several years ago before I found Dr. Peat when I was struggling with hair loss, but I had no idea what pregnenolone and progesterone were, and the whole theory went over my head.

 

[Lokzo]

Now that I think about it, raising cortisol very high (via caffeine) was what cured my hair loss

Caffeine raises other protective hormones haha, not just cortisol.

 

[Broco6679]

This would make sense why Adrenal Cortex does me wonders. I have extremely low cortisol production, and I find it really does help me with energy/mood.

I'm considering starting adrenal cortex too. Did you experience any benefits outside of improved mood and energy?

 

[Lokzo]

I'm considering starting adrenal cortex too. Did you experience any benefits outside of improved mood and energy?

Yeah it definitely helps my energy and blood pressure. I think I also noticed better appetite and digestion. Better strength/endurance in the gym too.

 

[Broco6679]

Yeah it definitely helps my energy and blood pressure. I think I also noticed better appetite and digestion. Better strength/endurance in the gym too.

Thanks! Can I ask why you decided to take it? Were your coritsol / DHEA-S levels low?

 

[Broco6679]

This thread interests me a lot. My hair loss started whilst on Testosterone Replacement Therapy, and I have a wide range of blood work over the last two years that correlate with the content of the op - high E2, low progesterone, high prolactin, low thyroid function w/ hypo symptoms, low end DHEA and extreme anxiety / fatigue.

Bloods on TRT:

Progesterone *0.59 nmol/L 0.70 - 4.30
Testosterone 28.5 nmol/L 8.64 - 29.00
Free Testosterone - Calc 0.55 nmol/L 0.20 - 0.62
Oestradiol *162 pmol/L 41.00 - 159.00
SHBG 38.9 nmol/L 18.30 - 54.10
Prolactin 314 mIU/L 86.00 - 324.00
fT3 5.16 pmol/L 3.10 - 6.80
fT4 14.200 pmol/L 12.00 - 22.00
TSH 2.53 mIU/L 0.27 - 4.20

Those bloods seem to agree with the OP. I've now come off of TRT and my bloods look much better, though still not optimal:

FSH X 1.34 IU/L (Range: 1.5 - 12.4)
LH 5.27 IU/L (Range: 1.7 - 8.6)
Oestradiol 75.1 pmol/L (Range: 41 - 159)
Testosterone 20.2 nmol/L (Range: 8.64 - 29)
Free Testosterone - Calc. 0.419 nmol/L (Range: 0.2 - 0.62)
Free Androgen Index 65.8 Ratio (Range: 24 - 104)
Prolactin 112 mU/L (Range: 86 - 324)
DHEA Sulphate 7.780 umol/L (Range: 5.73 - 13.4)
TSH 2 mIU/L (Range: 0.27 - 4.2)
Free T3 4.76 pmol/L (Range: 3.1 - 6.8)
Free Thyroxine 16.700 pmol/L (Range: 12 - 22)

Prolactin and estradiol both reduced massively, and testosterone recovered well - my levels are much higher now than they ever were Pre-TRT. Thyroid function remains poor with an elevated TSH and below mid-range fT3/4 and persisting symptoms of hypo. I haven't had progesterone checked sine coming off.

I'm going to begin taking adrenal cortex glandular to support DHEA and coritosl levels. After ~2 weeks I am going to begin taking NDT, starting with an extremely small dose and slowly increasing until hypo symptoms are no longer present (cold hands and feet, low pulse, low oral temps, thinning hair and outer eyebrows etc).

I'll update this thread if I see any improvement with my hair. My hair loss is in a diffuse pattern, though it is only located on top. I lose an insane amount of hair each day - this is how much hair I lost after rubbing my head for 2 minutes over the sink:
Imgur

My eyebrows are also starting to thin significantly as well.

I would ideally take pregnenolone instead of adrenal cortex, but when I take it my veins begin to swell and enlarge, almost as if they're becoming varicose.

I'll be getting bloods throughout this process to monitor thyroid, adrenal and sex hormone function throughout.

 

[Lokzo]

Thanks! Can I ask why you decided to take it? Were your coritsol / DHEA-S levels low?

I had lower metabolised cortisol according to the DUTCH test.

 

[Peater Pan]

came across this thread thanks to @tallglass13 . its funny because my confusion is about why adrenal cortex (a cortisol raising supplement) helps me tolerate T3, is completely answered in this guys post. i accept that I seem to be in a minority, most people seem fine taking t3 without raising cortisol, but all i can say is it works. so whether or not ray agrees with it, what this guy is suggesting, as bro-sciency as it is, is completely spot on in my experience. Some of us do need to raise cortisol in order to tolerate and be able to use T3. And if you look at the Stop the thyroid madness groups, who have interacted with hundreds of thousands of thyroid users, they have whole pages dedicated to the importance of raising cortisol in order to tolerate t3. interestingly i emailed ray about this adrenal cortex/cortisol query the other day and its the first time he didnt reply to me. i dont think its his favourite topic.

My take away from speed reading it is that progesterone can do the same, no?
Pregnenolone may be making things worse for me for lack of T4?

"2c) If pregnenolone doesn’t deliver adequate cortisol, then either:
……(i) you may need to supplement with both pregnenolone and biotin, since biotin is a cofactor used by adrenal enzymes to synthesize cortisol from pregnenolone
……(ii) you may need to supplement with pregnenolone and thyroid hormones T4 and T3 concurrently, since your adrenal enzymes may just be sluggish, and your hypothalamus won’t allow you to increase your thyroid T4 levels [see next section re how to do this]
……(iii) if the ab"ove two options don’t work, then you can’t help pregnenolone synthesize into cortisol, and you need to supplement with either progesterone, 17 hydroxyprogesterone or cortisol (as hydrocortisone = man made bioidentical cortisol) because your adrenal enzymes will allow one of these to synthesize into cortisol.