Hormones And Hairloss

Raincoast · Mar 25, 2017

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

redlight · Mar 25, 2017

do you have the contact info for chilln?

mayweatherking · Mar 25, 2017

I sent an extract of chillns work to ray to ask him about it.. ray was basically Savage and said he had no idea what he was talking about and his view on hormones was rooted in no real knowledge or something along those lines

tallglass13 · Mar 25, 2017

I would be interested if @haidut, @tyw , and any other smart forum members can conquer with this....

Raincoast · Mar 26, 2017

I posted my experiences with preg/t4/t3 in a separate thread in labs/bloodwork.
My results seem like they could fit in with the theory above.

Here's another interesting one,

Thyroid Boost 101 (chilln)
IF YOUR CORTISOL IS TOO LOW, YOU ARE GUARANTEED TO BE HYPOTHYROIDHypothyroid symptoms most likely translate into the fact that you need pregnenolone to boost your neurotransmitters and cortisol before boosting thyroid hormone T3.

This is because thyroid hormone T3 only works to boost overall metabolic rate when there’s sufficient cortisol present to work with that thryoid hromone T3 to complete the metabolism boost.

Thryoid hormone works synergistically with cortisol to achieve the boost in overall metabolism which is incorrectly attributed to thryoid hormone T3 alone.

Ie: if your body is already too low on pregenolone and neurotransmitters and cortisol, then you will guaranteed also be hypothyroid, because your existing thyroid hormone T3 cannot find enough cortisol to “buddy up” and get the job done of increasing overall metabolism.

So if someone with too low pregnenolone and neurotansmitters and cortisol were to try boosting their thyroid hormone T3, then the results would make them feel even worse that they do now, because the supplementary thyroid hormone T3 they put into their body would soak up most of their last remaining cortisol reserves and then they would truly in a bad way, because our body doesn’t have any long term storage forms of cortisol avialable to draw from to work with thyroid hormone to maintain our metabolic rate, and so our systems start to shut down, starting with our “will to do work”.

HOW DO THYROID HORMONES GET DYSFUNCTIONAL ?

This is usually due to the genetically triggered reduction in the setpoint of our overall metabolic rate (a big part of genetic aging), which has severe consequences such as:
a) downregulation of our cortisol-production-line,
b) downregulation of our testosterone-production-line,
c) downregulation of our ability to synthesize energy from body fat stores

The downregulation of our cortisol-production-line has severe consequences on the levels of our pregnenolone, which results is reduced levels of neurotransmitters. It’s this downreuglation of neurotransmitters which results in our brain’s inability to manage the competing requirements of energy metabolism and repairs.

Temporary causes of too low levels of neurotransmitters are: illness, or self inflicted via prescription neurotransmitter modulators, or exhaustion of neurotransmitters due to overtraining for competitive sports.

Too low levels of neurotransmitters causes our hypothalamus to mismanage CRH (cortisol release hormone), which cause our pituitary to mismanage ACTH, which causes too low levels of pregnenolone, neurotransmitters and cortisol,

Too low levels of neurotransmitters causes our hypothalamus to mismanage TRH (thyrotropin releasing hormone) which causes our pituitary to mismange TSH (thyrotropin stimulating hormone) which causes inadequate levels of thyroid hormone T3.

Too low levels of neurotransmitters causes our parasympathetic nervous system to mismanage the feedback signals from D1 enzyme regulation within cells. (D1 enzymes convert T4 into T3).

Finally genetically triggered age-related-hormonal-decline downregulates our genetic setpoint for overall metabolic rate. So the older we get, if we only restore our neurotransmitters to former optimum youthful levels, that is not going to restore our overall metabolic rate to its former youthful levels.

SYMPTOMS OF HYPOTHYROIDISM

If we are allowing ourselves to grow old gracefully, and we refuse to push ourselves beyond our body’s reducing limitations, then the symptoms of hypothyroidism are simply “slowing down and feeling colder”.

If you’re that sort of person, then stop reading this post now.

If you are pushing yourself beyond your aging body’s limitations, then the symptoms of hypothyroidism are as follows:

Mandatory either:
1) low or normal serum TSH, resulting in too low T3
Mandatory or:
2) too low salivary cortisol (on a 4-times-per-day test)
Mandatory or:
3) too high reverse T3

Optional:
4) occasionally feel cold, and you still have some body fat which isn’t being metabolized to keep you warm

WHAT’S ALL THIS ABOUT HIGH REVERSE T3

When we push ourselves beyond the limits of our neurotransmitters and hormones, or when we age and our clock genes downregulate our resting metabolic rate significantly, then our hypothalamus downregulates our max leptin levels, which triggers a reduction in both cortisol and thyroid hormone metabolism, and in some people the reduction in thyroid hormone metabolism manifests as an increase in synthesis of T4 into RT3.

There’s currently no reliable mechanism to restore leptin sensitivity and max leptin levels, therefore there’s no optimum solution.

Our best workaround solution is the 3rd Generation Male Treatment Plan – which is discussed in detail in Hormone Modulation Therapy 101 – scroll down to “Implementing the 3rd Generation Male Treatment Plan”.

This treatment plan restores youthful resting metabolic rate without restoring leptin metabolism to optimal, yet it achieves decent results even though the efficiency is not 100%. This is because the 3rd Generation Male Treatment Plan doesn’t restore leptin sensitivity to youthful and doesn’t restore leptin max levels to youthful, therefore the body will still continue to store too much fat, but thankfuly the higher resting metabolic rate burns that fat off as fast as its accumulated.

What would be more efficient would be to restore leptin sensitivity and leptim max levels, and then the body would shunt glucose to cells to be metabolized for fuel rather than store the glucose as fat, and then burn the fat as fuel. That’s in the future.

Right now we have the 3rd Generation Male Treatment Plan, and it works pretty good.

MONITORING THYROID HORMONE METABOLISM

We wish to monitor our thyroid hormone’s contribution to our overall metabolic rate, the most reliable indicator is a set of several thyroid hormones. Ie: we cannot use just one of the following – we must use the whole set (bummer).

[ Attempts have been made to use either metabolic rate and / or body temperatures, to assess thyroid hormone metabolism. Since neither of these can be used to determine which hormones need modulation, therefore thyroid hormone labs are still necessary, therefore the additional time or expense in monitoring metabolic rate, or body temperature, yields very low return on effort. ]

The reason why measuring body temperature is not a useful indicator of any specific thyroid hormone, is because the body has temperature compensation mechanisms built in which use sweat (evaporation), thermal radiation, and sugar burn.

It takes far more technology than we can muster in 2010 to measure and correctly account for the effects of these thermal compensation mechanisms, in order to attrubute a change in temperature to a reasonably precise level of any thyroid hormone.

###

By monitoring the following hormone levels, and pregnenolone and cortisol, we can reverse engineer which of the above situations is causing thyroid hormone dysfunction:

a) thyroid hormone antibodies, ie: thyroglobulin antibodies, and thyroid peroxidase antibodies, and TSH antibodies.
b) free T3
c) free T4
d) reverse T3 <— CRITICAL
e) TSH
f) total T3 <— not critical, but still helpful
g) total T4 <— not critical, but still helpful

TREATMENT OPTIONS FOR HYPOTHYROIDISM (INCLUDES TOO HIGH REVERSE T3)
Executive Summary

The methods of boosting thyroid hormone are:
a) Supplement with iodine / iodide, selenium, Vit D3 if your diet has lost these since you were a younger and healthier man [ can be detrimental if your antibodies are high ]
b) Supplement with thyroid hormone T4 (takes around 2 weeks to stabilize serum levels, due to extremely long half life) [ can be detrimental if your antibodies are high ]
c) Supplement with thyroid hormone T3 in slow release form (I recommend this when getting started) which is effective for a max of around 6 hours, so there’s no long term effects if you accidentally dose too high (in which case take a 5mg tab of HC).

TREATMENT OPTIONS FOR HYPOTHYROIDISM (INCLUDES TOO HIGH REVERSE T3)
Details

1) Crticial vitamins and minerals

1a) Ensure adequate selenium and iodone and vitamin D, not to “overdrive” levels.

1b) Monitor improvement in T4 -> T3 conversion, versus T4 -> reverse T3 conversion.

2) Boost cortisol

2a) Ensure plenty of pregnenolone <– citical

2b) Confirm adequate cortisol (due to pregnenolone boost) <– citical

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 above 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.

2d) Monitor improvement in T4 -> T3 conversion, versus T4 -> reverse T3 conversion.

PREGENOLONE IS CRITICAL TO ENSURE ADEQUATE NEUROTRANSMITTERS TO ENSURE THE BRAIN CAN MANAGE THE MONITORING OF METABOLISM FUNCTIONS AND CAN COORDINATE D1 ENZYME ACTIVITY IN PERIPEHERAL TISSUES

CORTISOL IS CRITICAL BECAUSE THYROID HORMONE T3 AND CORTISOL WORK SYNERGISTICALLY TO CREATE THE BOOST IN METABOLISM WHICH IS INCORRECTLY ATTRIBUTED TO THYROID HOROMONE T3 ALONE

3) If thyroid antibodies are low, boost thyroid hormones T4 and T3

3a) If thyroid antibodies are low, and if it works for you, then you supplement with dosages of iodone and potassium iodide are much greater than necessary to correct any iodine / iodide deficiency. This way, the dosages of iodone and iodide force the production of more T4 and force the synthesis of T3 from T4.

Very few of us experience less-than-beneficial side effects from this use of iodine an diodide. Many experience digestion upset at too large doses, because iodine interferes with digestion. So don’t dose greater than your digestion can handle.

Those of us with excessive thyroid auto immune issues occasionally experience a degradation of symptoms when trialling these larger doses of iodine an iodide, so those with hashimoto’s issues should ensure their medical professional adviser sets up an iodoral trial very carefully.

3b) If thyroid antibodies are low, and if you have years of experimentation time, then boost thyroid hormone T4 and T3 output via herbs:

Some people spend years looking for a herb which consistently upregulates their metabolic rate. Some find that maca delivers. Most don’t.

But there are a hundred other herbs which some people have found works specifically for them. Not one of the herbs works reliably in everyone to upregulate overall metabolic rate.
If you want to use herbs to do this you might get lucky in one day, or never. Good luck.

3c) If thyroid antibodies are low, and you prefer a speedy solution, then boost thyroid hormones T4 and T3 via a mix of T4 and T3 supplementation, but best to start out with T3 only because you have much better control over short term excesses than with T4.

The most reliable way to boost thyroid hormones is via direct supplementation with thyroid hormones T4 and T3. Provided there is adequate cortisol, and provided you’re only trying to boost your overall metabolic rate to optimum, no more, then this method is almost guaranteed to work in everyone.

The most common choice is a pig glandular extract such as any of:
(i) armour thyroid
(ii) westhroid, west thyroid
(iii) naturthroid, nature thyroid
(iv) erfa
… all of which contain a mix of both T4 and T3 (and several other less well researched thyroid hormones).

One way to gradually learn how your body responds to thyroid hormone supplementation is to initially avoid T4 and supplement only with slow release T3. This is helpful because T4 has a half life of several days, so if you take too much T4 then it will take around 2 weeks to elimiate the excess normally, or you will need to boost your cortisol high during the day to metabolize the excess T4 faster (and you will feel hotter if you do this).

Once you become accustomed to how your body handles slow release T3, then may discover that you still need relatively frequent dosing to keep your T3 levels sufficiently high all day (and partially into the night too). That’s when it’s time to replace as much of your T3 with some T4 as you can – eg: via some armour thyroid. The very long half life of T4 (several days) will result in once-per-day dosing, or at most twice-per-day dosing.

More specific dosing suggestions for T3-only, and T4-only, are provided further below.

4) If thyroid antibodies are still high, boost thyroid hormone T3 only (pref slow release T3)

Normally thyroid antibodies are quelled by optimizing digestion, which usually occurs simply by improving corotisol levels.

If thyroid antibodies remain stubbornly high, then try to eliminate foods such as gluten, ie: you may have a gluten sensitivity.

When thyroid hormone anitbodies are high, then boosting T4 aggravates those antibodies, but boosting T3 does not.

But thyroid hormone T3 has a half life in serum of only a few hours, therefore there needs to be a way to extend the time the T3 is available, and the best way to achieve that is to get T3 compounded with methocel (TM) (methocel = methylcellulose or hypromellose) as slow release T3.

DOSING SUGGESTIONS FOR T3-ONLY, AND T4-ONLY
Dosing suggestions for T3-only, and T4-only

When dosing T3 without any T4, and when dosing T4 without any T3, consider the following:

Only ever start at a known ‘too low’ dose, and then incrementally increase the dose until you get to your optimum based on the combination of labs, symptoms, and understand of hormone biology – and back off as soon as you experience any adverse effects.

If you experience any adverse effects then if your resting metabolic rate needs a boost, then boosting your cortsol will allow you to increase your dose of thyroid hormones. If your resting metabolic rate does not need an increase, then do not attempt to increase your thyroid hormone dose by boosting your cortisol – this is because the increase to your resting metabolic rate may cause detrimental health issues.

For T3 (without any T4) this dose range is 5 micrograms to 60 micrograms per dose, up to 6 times per day <– only hyper metabolizers of T3 can consider 60 micrograms of T3 per dose to be their upper limit, no-one else should go anywhere near that dose of T3-only.

Those whose cortisol is very very low will discover that even 5 micrograms of T3 will cause irregular heart beat. In other words, there is no such concept as a minimum safe effective dose of T3 which everyone can consider trivial.

For T4 (without any T3) this dose range is 40 micrograms to 600 micrograms, daily <– only hyper metabolizers of T4 can consider 600 micrograms of T4 to be their upper limit, no-one else should go anywhere near that dose of T4 -only.

NB: The only reason 40 micrograms of T4 is considered a minimum relatively safe dose of T4 is because those whose cortisol is very very low should be able to synthesize this amount of T4 entirely into reverse T3, which is inert.

PREGNENOLONE LOSES ABILITY TO SYNTHESIZE INTO CORTISOL WHEN T4 RUNS OUT

This happens if your rate of T4 production is too low.

By boosting your cortisol (via preg supplementation) you’re allowing your cortisol to work synergistically with your thyroid hormones to boost your overall metabolic rate.

So your cells (which have their own ability to regulate D1 enzymes) really do want to boost their overall metabolic rate when there’senough cortisol hanging around, and will synthesize T3 from the available T4 to maintain that (nice and) high overall metabolic rate.

But if your hypothalamus doesn’t trigger more TRH, to trigger the pituitary to produce TSH, to trigger the thyroid to produce more T4, then you cells will run out of T4.

Our hypothalamus limits our TRH based on its genetic aging program. There is no one-time-only mechanism to reverse the hypothalamus’s genetic aging program. But there are two main workarounds:
a) herbs
and
b) thyroid hormone supplementation.

Copyright is retained by chilln, 2008, 2009, 2010, 2011

Thyroid Boost 101 (chilln)
Tagged on: hyperthyroidism hypothyroidism thyroid
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tallglass13 · Apr 2, 2017

Excellent stuff thank you

Scenes · Apr 9, 2017

Raincoast said:
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

So is there any merit to this? @TubZy @haidut @sladerunner69 or anyone who knows their stuff.

Basically suggests taking prog/preg and t3 will regrow hair, but they need to be taken in sync. Says MPB is caused by too LOW cortisol and too low progesterone.

Also suggests blocking dht topically (not systemically) is useful.

sladerunner69 · Apr 9, 2017

mayweatherking said:
I sent an extract of chillns work to ray to ask him about it.. ray was basically Savage and said he had no idea what he was talking about and his view on hormones was rooted in no real knowledge or something along those lines

Yeah I don't see any tangible evidence of cortisol being beneficial to thyroid function in any literature, and I have always viewed as having an alternate/replacement relationship not a complimentary relationship

Can you post the email please?

mayweatherking · Apr 9, 2017

sladerunner69 · Apr 9, 2017

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.

Amazoniac · Apr 9, 2017

Effect of Exogenous Estrogens on the Male Mammal1 - ScienceDirect

Hair growth is retarded or even prevented by the administration of estrogen to the male (or female) mammal.

It's strange that when I tried to find the review searching on Google for the exact title no direct result appeared.

Raincoast · Apr 9, 2017

Another read to add to it...

Hormone-related guidance – thyroid, testosterone, estrogen, coristol, etc

Testosterone Boost 101 (chilln)

SAFE METHODS TO BOOST TESTOSTERONE

There are many many safe-in-the-long-term therapies to boost testosterone.

Here’s the list – I personally recommend option “a)” above all others.

a) chilln’s favorite Boost resting metabolic rate, which genetically reprograms all of our cells (for the duration of the increase in resting metabolic rate) to tolerate higher serum levels of all hormones, which includes testosterone, without taking evasive actions typical of excessive hormone metabolism (such as creating excess SHBG, or creating excess E2).

b) Promote lots of stage 3 deep sleep, there’s many ways to achieve this, eg: address any unresolved sleep apnea, reduce / remove caffeine towards the latter half of the day. Too high and too low cortisol detrimentally affects sleep. See a) above.

c) Manage too high cortisol back to optimum, since too high cortisol downregulates T (testosterone) and GH (growth hormone) by more than is optimal for long term health – eg: reduce physical and mental stressors

Managing too high cortisol is explained in detail in Cortisol Reduction 101

d) Switch out, or wean off, the supplementation of any drugs which suppress T or DHT such as finasteride, accutane, many diuretics, some neurotransmitter re-uptake inhibitors, statins, there’s many more.

e) Switch out, or wean off, the supplementation of over-the-counter supplements which raise E2 in males, such as DHEA (in males who don’t need supplementary DHEA!)

f) Switch out, or wean off, the supplementation of over-the-counter supplements which have estrogenic effects in males, eg: soy isoflavones.

g) Undergo surgical correction of any varicocele venous obstructions in the scrotom.
http://www.varicocoele.com/diagnosis_varicocele.htm
…(i) embolization <— less reliable, lower cost
…(ii) microsurgery removal <– more reliable, higher cost

i) Optimize diet to remove foods which promote metabolic syndrome (ie: high GI carbs)

j) Boost T via a “restart” using either:
….(i) experimetnal triptorelin (Dr Crisler only at this stage)
….(ii) from one week to several months of low dose clomid or tamoxifen
….No matter which method is used, testosterone is only restored to your age-appropriate levels, ie: restarts are pretty pointless in aged males.

k) Boost T via supplementary HCG as monotherapy.

l) Boost T via supplementary T, as transdermal bioidentical T.

m) Boost T via supplementary T, as intramuscular injected T esters (eg: testosterone cypionate) which convert to bioidentical T

n) Boost T via E2 (estradiol) reduction, using arimidex <— only works for a very small minority.

o) Boost T via E2 reduction, using DIM <— only works for a very small minority.

p) Some combinations (not all combinations) of the above, are more effective than just one of the above approaches.

That’s it.

Of course there’s a million people trying a million other therapies, and all of them carry high risk.

BOOSTING RESTING METABOLIC RATE

From Hormone Modulation Therapy 101

Genetic aging’s predominant effect which forces the gradual reduction in our hormone levels as we age, is the relentless downregulation of our resting metabolic rate.

Our resting metabolic rate is our minimum metabolic rate, and we notice it when we’re lounging around, not doing much, eg: relaxing on a beach while on vacation, or watching a boring movie on TV.

Our hormone levels are most strongly dependent on our resting metabolic rate, ie:
a) the higher our resting metabolic rate, then our hypothalamus will allow our hormone levels to be higher – and this is our optimum youthful situation.
b) the lower our resting metabolic rate, then our hypothalamus will force our hormone levels to be lower – this gets worse and worse the older we get.

In other words, the most profound thing we can do to restore most of our hormone levels back to youthful, is to restore our resting metabolic rate so that our hypothalamus will allow ALL our hormones to operate at higher levels through the day, without experiencing any symptoms of excess of any hormones.

The process of boosting resting metabolic rate is explained in Hormone Modulation Therapy 101 – scroll down to “What process should my doctor follow…”.

INJECTED VERSUS TRANSDERMAL T

The primary driver behind the decision of people to choose transdermal T versus injected T esters is the misconception that in all cases, switching from transdermal T to intramuscular injected T ester (testosterone cypionate) is necessary to reduce E2 levels.

The degree of aromatization of transdermal testosterone is a function of :

a) how fast you absorb transdermal T
……this is dependant on T dose and the base,
……the faster you absorb T, the more likely it is to cause aromatization if your cortisol can’t ramp up enough to downregulate the increase in T metabolism

b) your body fat content
……your body fat is an estrogen generation factory)

c) the ability of your body to ramp up your cortisol-production-line to downregulate your T
……we are much much better off when our body can downregulate our T metabolism using cortisol, otherwise it will aromatise T into E2 and downregulate T using E2.

The degree of aromatization of intramuscular injected T cypionate testosterone is a function of :

a) how fast your IM injected T cypionate converts into T
……this is dependant on T dose,
……the faster you absorb T, the more likely it is to cause aromatization if your cortisol can’t ramp up enough to downregulate the increase in T metabolism

b) your body fat content
……your body fat is an estrogen generation factory)

c) the ability of your body to ramp up your cortisol-production-line to downregulate your T
……we are much much better off when our body can downregulate our T metabolism using cortisol, otherwise it will aromatise T into E2 and downregulate T using E2.

##########

That the only differentiator in the two scenarios is:
a) how fast you absorb transdermal T
……this is dependant on T dose, and the carrier used,
versus:
a) how fast your IM injected T cypionate converts into T
……this is dependant on T dose.

The comparison of these two situations is way too complex to be achieved theoretically, so you and your medical professional adviser will need to do some therapeutic trials (dosage response trials) to determine the outcomes.

TESTOSTERONE METABOLISMS

T metabolism is the rate that all of the following molecules trigger a receptor, successfully enter the cell, and then trigger additional activity:
a) (most effect) testosterone
b) (least effect) testosterone-bound-to-SHBG ( triggers “megalin” receptors )
c) (medium effect) resting metabolic rate ( regulated by thyroid hormones, cortisol, insulin )

DHT metabolism is the rate that all of the following molecules trigger a receptor, successfully enter the cell, and then trigger additional activity:
a) (most effect) dihydrotestosterone
b) (least effect) dihydrotestosterone-bound-to-SHBG ( triggers “megalin” receptors )
c) (medium effect) resting metabolic rate ( regulated by thyroid hormones, cortisol, insulin )

Combined T metabolism is the rate that all of the following molecules trigger a receptor, successfully enter the cell, and then trigger additional activity:
a) (most effect) testosterone
b) (least effect) testosterone-bound-to-SHBG ( triggers “megalin” receptors )
c) (most effect) dihydrotestosterone
d) (least effect) dihydrotestosterone-bound-to-SHBG ( triggers “megalin” receptors )
e) (medium effect) resting metabolic rate ( regulated by thyroid hormones, cortisol, insulin )

There are no defined units for any testosterone metabolism functions. This is because no-one has even agreed how to perform direct measurements of our testosterone metabolism.

Our T metabolism is upregulated by free T, T-bound-to-SHBG, resting metabolic rate.

Our DHT metabolism is upregulated by free DHT, DHT-bound-to-SHBG, resting metabolic rate.

Our T and DHT metabolisms are strongly downregulated by SHBG, progesterone and cortisol.
* SHBG binds to testosterone, and SHBG-bound-to-testosterone dissociates so slowly that it’s effectively “out of service”.
* Progesterone competes with T and DHT for androgen receptors. When progesterone fils an androgen receptor, the cells T or DHT metabolism does not increase.
* Cortisol interacts with a cell’s genes to limit the effectiveness of T and DHT’s ability to trigger genetic actions.

And these are only the strongest inputs to our T and DHT metabolisms. There are several weaker inputs too, which we must overlook for pragmatic reasons.

Since we must overlook some numeric inputs, therefore we cannot measure our T metabolism absolutely, and so we must include a symptoms analysis to confirm that we can explain most of our symptoms just using the strongest influencing substances.

Here’s the list of measurements we use to determine our T metabolism:
…..a) labs for the components which modify our T metabolism
………(i) serum total T, SHBG and albumin (we prefer bioavailable T)
………(ii) serum total E2 and SHBG
………(iii) salivary 4-times-per-day cortisol
………(iv) serum progesterone <— optional, but preferable
………(v) serum pregnenolone <— optional, but preferable
…..b) the symptoms of each of the components which strongly influence our T metabolism
………(i) damage tolerance (all hormones contribute)
………(ii) erection performance (all hormones contribute)
………(iii) energy levels (cortisol mostly)
………(iv) brain fade (pregnenolone mostly)
………(v) hairiness and baldness (DHT and progesterone mostly)

Including DHT metabolism is far more complex, and I just don’t have the time to write it up for you. You’ll need to work out how to include DHT metabolism for yourself.

WHY IS MY TESTOSTERONE LOW, AND / OR MY E2 HIGH, AND / OR MY SHBG HIGH ?
Why is my testosterone low, and / or my E2 high, and / or my SHBG high ?

Background:
T = testosterone
T serum levels <–versus–> T metabolism
DHT serum levels <–versus–> DHT metabolism, and Combined T metabolism
Our Cortisol-production-line, E2 and SHBG all strongly downregulate T

* T metabolism, DHT metabolism and combined T metabolism were explained in the previous section. That info is critical to understanding what’s being explained here.

* Males only make E2 from T via the action of aromatase enzymes, not other way.

* Males only make DHT from T via the action of 5-alpha-reductase enzymes, no other way.

* Our livers make most of our SHBG, but some is produced by the testes, and testes-produced SHBG is a sub-category of SHBG called ABP (androgen binding protein).

* When we’re young, our youthful resting metabolic rate is high, and this programs our genes in every single one of our cells (includes hypothalamus) to tolerate high levels of all hormones, not just testosterone.

* When we’re young, our youthful combined T metabolism is continually balancing under the control of the hypothalamus and pituitary gland in our brain. Ie: the factors which upregulate our combined T metabolism (T, T-bound-to-SHBG, DHT, SHT-bound-to-SHBG) are continually opposed by the factors which downregulate our T metabolism (SHBG, albumin, pregnenolone+progesterone+17 hydroxyprogesterone+cortisol).

Genetic Aging:
Downregulation Of Resting Metabolic Rate
Nasty Consequences For Testosterone and DHT

* Between the age of 20 and 30, our resting metabolic rate gets downregulated by clock genes, this is not a result of genetic damage. If you’re over 30, no doubt you realize that you quickly lost the ability of your body to recover from stress or exertion as fast as it used to. This is true even if your diet and health maintenance were absolutely optimum.

* As we age, the numbers of our leydig cells decline, so our body has less and less T to maintain our combined T metabolism. Since DHT is much more strongly androgenic than T, therefore our body increases the relative proportion of DHT, in order to maintain our combined T metabolism.

* We know that this loss in damage tolerance between age 20 and 30 is hormone related, because when we restore those hormone levels to their former youthful levels, we recover most of that youthful damage tolerance.

* This genetic reduction in our resting metabolic rate (between ages 20 and 30) also directly downregulates our energy metabolism, which is the synergistic interaction of our cortisol + thyroid + insulin subsystems. The downregulation of our cortisol-production-line hormones (eg: preg, prog, cortisol) is most debilitating for males, because our “drive” uses up our cortisol reserves much more quickly than women, so when our cortisol is genetically lowered, we actually experience cortisol exhaustion (commonly termed “adrenal fatigue” but this is a very poor term since cortisol exhaustion occurs because our hypothalamus limits our max cortisol levels due to genetic aging, NOT because our adrenals are “worn out”).

* The genetic downregulation of our cortisol-production-line creates the nasty effect of removing a strong downregulator of our combined T metabolism. As a result our body must take “evasive action” and switches to using increased levels of E2 to keep our combined T metabolism constant (downregulated). It does this by synthesizing more E2 from T.

* When our body downregulates our cortisol-production-line, we are left with less pregnenolone and less progesterone than in our youth, which means our neurotransmitter levels suffer, and the balance of those neurotransmitters is less able to provide optimum orgasms, and less able to maintain an erection for long durations.

* Boosting our cortisol-production-line via hormone modulation therapy forces the body to reduce E2 and reduce high SHBG, so that the forces which are downregulating T remain constant. The benefit is that we recover our optimum neurotransmitter balance for optimum erection and orgasm performance.

* Boosting our cortisol-production-line requires a detailed investigation, and is the subject of the primer Cortisol Boost 101.

* Independently from the above issues relating to progesterone, cortisol and testosterone, the genetic reduction in our resting metabolic rate (between ages 20 and 30) reprograms all of our genes to tolerate reduced levels of all of our hormones, and that includes testosterone. The effect of this is:

** Some male’s livers then increase SHBG to further downregulate T levels, and thus T metabolism (ouch!).

** Some male’s cells then further increase E2, to further downregulate T levels and thus T metabolism (ouch!).

*** Using arimidex to suppress E2, or using nettle root or danazol to manage SHBG, dostinex to manage prolactin, or using finasteride or avodart to manage DHT, in order to manage erection performance and / or orgasm performance, only works in relatively young males whose resting metabolic rate has not yet been downregulated much. Once our genetic aging has downregulated our resting metabolic rate considerably (usually around age 40) then this method of suppressing E2, SHBG and / or DHT is a rollercoaster ride which never stabilizes.

*** The reason that the method of suppressing E2, SHBG and / or DHT is a rollercoaster ride which never becomes stable is because our body implements two independent methods to downregulate T (1: cortisol-production-line hormones, 2: resting metabolic rate) and every time we specifically suppress E2, SHBG and / or DHT, we also increase resting metabolic rate by a different amount, and so the two “forces” conflict, but they don’t cancel each other – and one of them dominates.

As a result, the only reliable solution to increase T levels and thus T metabolism (and thus keep estrogens optimum, DHT optimum, and SHBG optimum) is to:
a) boost our resting metabolic rate back to youthful, so our youthful genetic program kicks in once more, and allows higher levels of all hormones not just T
and
b) let the hypothalamus manage T metabolism at close to its genetic setpoint for optimum T, using it’s preferred main downregulator, ie: the cortisol-production-line hormones (eg: preg, prog, cortisol).
and
c) Both a) and b) are achieved by the combination of:
….(i) boosting the cortisol-production-line hormones (eg: preg, prog, cortisol) back to more youthful levels
….(ii) booting the thyroid hormones (eg: T3, T4) back to more youthful levels.

How to achieve this is explained in the Hormone Modulation Therapy 101 primer – scroll down to “What process should my doctor follow…”

HORMONE FEEDBACK AND SHUTDOWN

If we males supplements with just a little T, our body will simply produce less testicular produced testosterone to compensate, so our T levels will return to where they were at the outset.

If we supplement with a mid-level of T, our body will completely stop producing testicular produced testosterone to compensate, so our T levels will return to where they were at the outset.

If we supplement with a lot of T, our body will completely stop producing testicular produced testosterone, but it won’t be able to compensate, and finally we’ll have more T than we did before we started, but now our testicles will be shutdown.

As a result, a testosterone hormone modulation therapy protocol which uses supplements must force our testicles to produce T, ie: via HCG, as well as supplement with some additional T as either a transdermal gel, or as an injected T ester (T cypionate injected into muscle).

WHAT IF BOOSTING TESTOSTERONE BOOSTS E2 TOO HIGH ?

If this occurs, there’s four ways to address this problem:

Plan A is to reduce T levels to reduce E2. Only if you can’t find a reduced T level, where E2 is managed optimally, should you implement plan B.

Plan B is to boost T so that E2 levels are a little too high, then boost the cortisol-production-line (pregnenolone+progesterone+17 hydroxyprogesterone+cortisol), (usually via either a HCG boost or a transdermal pregnenolone boost). Boosting cortisol suppresses T metabolism even when serum total T levels remain constant. Boost cortisol until the reduction in T metabolism reduces E2 back to optimum.

Only opt for Plan C = arimidex after both plan A and plan B fail to achieve optimum E2.

An alternative to Plan C, for those who dislike Big Pharma drugs, is Plan D = boost GH, and reduce T.

GH is a repair trigger hormone with very similar activity to T (not 100% overlap) and thus bo boosting T, we get our repairs triggered, so we can reduce our T by a comparable amount, and by reducing T, we reduce our E2.

Since a small reduction in T usually results in a larger reduction in E2, we don’t have to reduce our T to be too low, in order to get our E2 optimized.

WHAT IF BOOSTING TESTOSTERONE (VIA HCG) SENDS CORTISOL TOO LOW ?

Using HCG to boost testosterone over many months, or a few years, can cause too low cortisol (fatigue and weakness) in some males (not all).

The reasons are as follows:

a) HCG upregulates two enzymes:
….(i) P450scc (cholesterol side chain cleavage enzyme), which synthesizes pregnenolone from LDL cholesterol
….(ii) 17β-HSD which synthesizes testosterone from androstenedione (and which synthesizes androstenediol from DHEA)

b) When the second set of reactions (ii) work faster than the first one (i), then there’s a deficit of pregnenolone. In this case the pregnenolone gets “stolen” from the cortisol-production-line !

c) Stealing pregnenolone from the cortisol production line initially causes the hypothalamus to upregulate CRH, which initially causes the pituitary to upregulate ACTH, which initially synthesizes even more pregnenolone from LDL cholesterol.

d) Either the hypothalamus or the pituitary cannot cope with this upregulation indefinitely (not sure why not) and one of them eventually packs it in, and then you get too low ACTH, and then you run out of pregnenolone on the cortisol production line, and you run out of cortisol too.

e) Running out of cortisol causes fatigue and weakness.

If you discover that your body is one of these which steal pregnenolone from the cortisol-production-line, then the workaround is to include some pregnenolone in your hormone modulation therapy regime.

The most reliable form of pregnenolone is transdermal pregnenolone, but some people get benefit from oral pregnenolone, or oral MLM (micronized lipid matrix) pregnenolone.

WHAT IF BOOSTING TESTOSTERONE SENDS DHT TOO HIGH ?

The fundamental reason for the increase in DHT in the first instance is due to lack of downregulation of T metabolism using either the cortisol-production-line hormones (eg: preg, prog, cortisol) which in turn is due to genetic downregulation and excessive stressors, or due to lack of E2, which is often due to the use of an aromatase inhibitor.

When we boost our cortisol-production-line hormones (eg: preg, prog, cortisol) we downregulate our T metabolism using the hypothalamus’s preferred method. Then our hypothalamus will automatically reduce E2 levels or else there would be too much downregulation of T metabolism.

When we “switch” the downregulation of T metabolism from “use E2 to downregulate T metabolism”, to “use the cortisol-production-line hormones to downregulate T metabolism”, then we get natural DHT control from progesterone (no need for avodart).

Progesterone is a part of the cortisol-production-line (ie: pregnenolone <–> progesterone -> 17 hydroxyprogesterone -> cortisol) and gets boosted when the cortisol-production-line gets boosted.

Progesterone competes with DHT for DHT receptors. When progesterone triggers a DHT receptor, and enters the cell, the progesterone molecule triggers progesterone actions, not DHT actions.

EXOGENOUS T VERSUS RESTARTING NATURAL T PRODUCTION
Exogenous T versus restarting natural T production

A restart involves using low dose clomiphene / Clomid or tamoxifen (both are SERM’s = selective estrogen receptor modulators) to suppress E2.

Clomiphene / Clomid has both E2 receptor blocking effects (E2 antagonist) and E2 promoting effects (agonist). The E2 receptor blocking effects restart the HPTA without the estrogen-agonist half blunting its effects.

Most benefit from as low as 10-20mg of clomiphene per day (not sure of optimum tamoxifen dose). You may need to run your restart for as long as six months, worst case, rather than increasing the dose.

It’s important to work your way up from a dose of clomiphene / Clomid which is a little too low, and then gradually increase it to find the minimum dose which restores your LH and testosterone levels.

Increasing the dose of clomiphene / Clomid or tamoxifen above your minimum dose definitely gets higher LH and testosterone levels, but rarely results in a restart of your natural production. Ie: when you need more than 20mg of clomiphene / Clomid then you run the risk that when you remove the clomiphene / Clomid and “unblock” your E2 receptors, then your hypothalamus will measure your E2 metabolism and determine that it’s too high, and so your hypothalamus will not maintain high GnRH, but will instead lower GnRH, which will lower LH which will lower testosterone.

Higher doses of clomiphene / Clomid or tamoxifen also result in the risk of permanent “floaters” in your eyes, which are due to too low E2 metabolic activity for too long.

###

Note that you can’t use serum E2 measurements as a biomarker for E2 metabolic activity, because clomiphene / Clomid and tamoxifen block E2 receptors, so serum E2 levels will be high when E2 metabolic activity is low.

###

A restart is rarely useful if you’re over 40, but even then only if:

1) If aging has not yet downregulated someone’s cortisol-production-line nor their testosterone-production-line, then that person will recover their youthful testosterone levels with a restart.

2) If aging has downregulated someone’s cortisol-production-line, but is has not yet downregulated their testosterone-production-line, then that person will recover their youthful testosterone levels with a restart, and only need to support their cortisol-production-line.

3) If aging has downregulated someone’s cortisol-production-line and their testosterone-production-line, then that person will not recover their youthful testosterone levels with a restart.

The older we get, eventually aging downregulates both our cortisol-production-line and our testosterone-production-line.

We can’t tell you, in advance, at what point in the aging process you are. Only a therapeutic trial using a restart will give you that info.

###

Sometimes simple clomiphene / Clomid / tamoxifen therapy fails to restore age-reduced T levels, or, sometimes T levels are restored, by fail to be maintained after removing clomiphene / Clomid / tamoxifen.

(remember that a restart will only restore your age-appropriate T levels. A restart will not restore your youthful T levels if you’re an aged male)

The reason a restart fails to generate enough T, or fails to “stick” once therapy is withdrawn, is usually because your resting metabolic rate was not boosted by the increased testosterone.

The reason you need your resting metabolic rate to increase, during a restart, is because our cells only tolerate higher T metabolism, when those same cells have a relatively high resting metabolic rate. When cells have a low resting metabolic rate, they treat high T metabolism as “excessive T metabolism”, and do everything in their genetic programming to reduce T metabolism to match their resting metabolic rate.

The workaround to this problem is to add hormones to increase resting metabolic rate. The way to achieve that is the 3 phase process explained in Hormone Modulation Therapy 101 – scroll down to “What process should my doctor follow”.

BOOSTING T CAN BOOST THYROID HORMONES AND RESTING METABOLIC RATE

Sometimes boost Thyroid hormone T3 can boost T levels, and sometimes boosting T can boost Thyroid hormone T3.

Here’s how boosting T levels can boost thyroid hormone T3 levels:

a) Initially T is too low, resulting in inadequate repairs, which causes increased inflammation.

b) Cortisol levels rise to suppress the inflammation.

c) Because cortisol is being used up to suppress inflammation, therefore there’s less cortisol to work with thyroid hormone T3 to boost resting metabolic rate.
Cortisol works synergistically with thyroid hormone T3, to boost resting metabolism. Thyroid hormone T3 cannot work independently from cortisol to boost metabolism.

d) Cells back off conversion of T4 into T3 because there’s less cortisol available to complete the boost in metabolism.

e) Boosting T at this point increases T metabolism, which results in triggering of repairs.

f) Repairs start being carried out, so now cortisol is no longer required to suppress inflammation, so cortisol serum levels rise a little.

g) Cells now absorb more cortisol from serum, so they start converting more thyroid hormone T4 into thyroid hormone T3, and the cell’s metabolic rate increases.

h) The rate of consumption of T4 increases, so the hypothalamus must increase TRH, which increases pituitary TSH, which increases the rate of T4 production (T4 levels don’t have to rise, although they usually do rise).

###

The reason this is not guaranteed to happen in all males who supplement with testosterone, is because some males consume cortisol faster than others, and those whose bodies consume cortisol fastest, are more likely to exhaust their cortisol before their thyroid hormones can maintain any increase in metabolic rate.

TESTOSTERONE INJECTIONS – ESTERS AND DISSOCIATION

Injecting testosterone means injecting a testosterone ester (ie: a testosterone molecule bound to an ester molecule), which is dissolved in oil, into a muscle.

All testosterone esters are inactive in the male body until the ester (eg: cypionate) is cleaved off by the esterase enzyme.

TESTOSTERONE INJECTION – HALF LIVES

The testosterone esters found in injectable products, all have different half lives to clearance (via urine and feces) ie:
a) Testosterone formate ………………….has an approx half life of 1.5 days in most people (not all)
b) Testosterone acetate ………………….has an approx half life of 3 days in most people (not all)
c) Testosterone propionate ………………has an approx half life of 4.5 days in most people (not all)
d) Testosterone enanthate ……………….has an approx half life of 6 days in most people (not all)
e) Testosterone cypionate ………………..has an approx half life of 8 days in most people (not all)
f) Testosterone undecanoate (Nebido) ..has an approx half life of 16.5 days in most people (not all)

Since each of us has varying metabolic rates, some of us will metabolize testosterone cypionate much quicker than the average, and will obtain a half life of only 4 days.

Each testosterone ester is mostly inert in the human body while the testosterone is still bound to the ester compound.
Testosterone-bound-to-an-ester-compound dissociates at a rate which results in the half lives per the above table.
The Testosterone-bound-to-an-ester-compound dissociates into testosterone, and the ester.
After dissociation, the testosterone is bioidentical to our testicular produced testosterone, and triggers all of the same biological activity as our testicular produced testosterone.

TESTOSTERONE INJECTIONS – STORAGE

Store your testosterone ester (eg: T cyp = testosterone cypionate) in the fridge at all times.
You can freeze testosterone, but it’s not going to add any value.

TESTOSTERONE INJECTIONS AND HCG INJECTIONS – SYRINGES

This syringe is what we recommend you use and it would fit your needs for both testosterone cypionate (which needs to be injected intramuscularly) and HCG (which needs to be injected subcutaneously).

BD Ultrafine II U-100 Insulin Syringe 31 Gauge 3/10cc 5/16 inch Short Needle 100/Box

—or if your thigh fat is just too thick to compress under 5/16 inch, then:
BD Ultrafine U-100 Insulin Syringe 30 Gauge 3/10cc 1/2 inch Needle 200/Box

These two syringes have short barrels. You can buy them online from hocks.com

TESTOSTERONE INJECTIONS – DOSING

Testosterone cypionate (T-cyp) is approximately 70% testosterone, the rest is the ester (cypionate) which is bound to the testosterone.

Therefore 100 mg T-cyp per week provides around 70 mg testosterone per week, or 10 mg testosterone per day. Our testicles manufacture up to 12 mg testosterone per day.

Usually testosterone cypionate comes at 200mg/mL density.
Double check and confirm your density is the same.

When the above syringe is loaded to the top (30 units) it has a volume of 0.3mL

On any size of insulin syringe one unit =0.01mL

0.3mL * 200mg/mL=60mg

Then inject this intramuscularly into your thighs. You’ll need to press hard enough to compress the fat above your thigh so that the 5/16 inch syringe penetrates into the muscle tissue.

###

Some complain that it takes 2 minutes to fill up above syringe with testosterone oil.
If you are press for time during shots,
pre-fill 5-10 syringes at your leisure time.

TESTOSTERONE INJECTIONS – INTRAMUSCULAR OR SUBCUTANEOUS

Injecting testosterone esters into the muscle tissue (IM = intra-muscular) of the thigh or buttocks is used by the majority.

Injecting testosterone esters subcutaneously (subQ = subcutaneous) was discouraged in the past due to very few members having only a few years experience with this form of administration. At this time we recommend you use a very cautious approach if you intend to inject your testosterone ester subQ instead of IM.
Injecting testosterone esters subcutaneously does indeed yield a satisfactory testosterone boost which is comparable to intramuscular injection, but this has not been formally assessed for safety over the long term (eg: decades).

Our short term knowledge of subcutaneously injected testosterone is as follows:

a) We need to inject testosterone subQ via small dosages either daily, or every second day, or every third day, because the volume of once-weekly injections typically results in leakage at the injection site.

b) Some testosterone ester formulations contain preservatives and / or carriers which cause irritation when injected subcutaneously, so you need to be on the look out for any irritation at the injection site.

c) There are two research papers assessing short term use of subcutaneously injected testosterone enanthate, over a few months, so if you prefer subQ injections to IM injections, then you may need to pass a copy of these papers to your medical professional adviser, ie:

Title: Men’s Health and Aging: The 5th World Congress on the Aging Male
Article number 51
Stable Testosterone levels Achieved With Subcutaneous Testosterone Injections
Journal: The Aging Male Jan 2006, Vol. 9, No. 1: page 15
Author(s): M.B. Greenspan, C.M. Chang
Abstract URL (USD $50 – this issue of this journal only contains abstracts, not full text)

and

Title: Subcutaneous administration of testosterone – a pilot study report
Journal: Saudi Med J. 2006 Dec;27(12):1843-6
Author(s): Abdullah M. Al-Futaisi, Ibrahim S. Al-Zakwani, Abdulaziz M. Almahrezi, David Morris.
Abstract URL
Full Text URL (free)

HCG LYOPHILIZED POWDER AND RECONSTITUTED LIQUID – STORAGE

You can store the lyophilized powder in both the fridge and freezer.

You can store the reconstituted HCG as liquid in the fridge, and it will not lose potency / efficiacy.

If you store HCG in the freezer, then it loses some potency / efficacy after defrosting, and this has been confirmed by those with a keen understanding of their hormone modulation therapy.

Those who use HCG exclusively for diet purposes have no way to quantitatively compare one HCG batch to another HCG batch, because hunger is a very subjective concept.

Those using HCG monotherapy to boost their testicular testosterone production all confirm that HCG loses an obvious amount of potency when it is defrosted after freezing in its reconstituted state. This noticeable difference may be lessend if the HCG is defrosted in the refrigerator instead of on a bench at room temperature. This hasn’t been reliably confirmed.

If you’re concerned about the stability and efficacy of urinary derived HCG, then switch to Ovidrel, which is recombinant HCG. One 250 microgram syringe of Ovidrel is equivalent to 6600 IU of urinary derived HCG. Thanks to Nuclear for that discovery.

I can guarantee Ovidrel lasts at least at least three months in the fridge when received unopened from the pharmacy, before diluting with water.

And it lasts at least another 2 months in the fridge after you’ve diluted it with water (even when that water is “water-for-injection” which has no preservative).

And if you need to travel then you can leave the diluted Ovidrel HCG at room temperature for a few days, and then put it in the fridge when you get to your destination, and you won’t notice any change in efficacy.

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The only people who can reliably vouch for the potency of HCG are those who use HCG monotherapy. The remaining people who use HCG in conjunction with exogenous testosterone have very little idea how much of their testosterone is derived from their testicles (via HCG) or from their T gel or injected T ester.

While several people claim they get good performance from reconstituted HCG after defrosting, they are not doing HCG monotherapy, and thus they have very little idea how much of their testosterone is derived from their testicles (via HCG) or from their T gel or injected T ester.

HCG INJECTIONS – DOSING

When using any type of testosterone you want to use also HCG to force your testicles to remain “on size”.

When injecting HCG, use around (350-400)iu/EOD EveryOtherDay (ie: :”EOD”)

Use the same syringes to inject T and HCG.
Two separate syringes.

We recommend you dissolve HCG in such a way that you end up with density of 2000iu/mL

We recommend you fill up your syringe up to the 20 unit mark to get 400iu=HCG=shot

Then inject this subcutaneously into the fat on your hips (love handles).

HCG INJECTIONS – FREQUENCY

How frequently you dose HCG requires that you know how long (as days or hours) a dose of HCG raises your T levels.

There are 3 ways to determine how long a dose of HCG raises your T levels:

1) chilln’s recommend method:

Overview:

This method uses a few weeks of HCG monotherapy to provide your body with the largest doses of HCG you’re likely to experience (a “monotherapy dose of HCG”). The largest doses of HCG will provide the longest duration increase in T levels. Then when you reduce the HCG and introduce exogenous T, you know for sure that the lower dose of HCG will raise your T levels for a shorter period of time than the monotherapy dose.

Method:

1a) If you’re starting out from a position where you don’t yet use any exogenous T, then start boosting your T using only HCG.

You may discover that you need to inject your HCG every second day, or daily, or even twice daily (as in my case) to get your T levels stable.

1b) If you’re already using both exogenous T and HCG, then gradually reduce your exogenous T and gradually increase the dose and frequency of your HCG injections, until you’re only boosting T with HCG.

You may discover that you need to inject your HCG every second day, or daily, or even twice daily (as in my case) to get your T levels stable.

This may take you from one to four weeks to make the switch, so be it.

2) Once you’re boosting your T via HCG monotherapy, your erection performance and orgasms may not be optimum because your testicles may have too few leydig cells remaining, or you may have a varicocele (which you will uncover via this therapeutic trial / dosage-response trial).

3) Once you’re boosting your T via HCG monotherapy, note how frequently you’re injecting your HCG. This is the longest time that HCG raises your T levels adequately. When your HCG levels are lower, then each dose of HCG will only raise your T levels substantially for less than this duration of time.

Initially choose a HCG injection frequency at daily, and then adjust your dosage to even out symptoms as much as possible (may not be perfect symptoms). Your medical professional adviser might start you at (say) 300 IU daily, but your daily optimum will not be 300 IU, and he needs to give you the freedom to adjust dosage up or down based on symptoms (all symptoms – T affects everything we do, usually via feedback with other critical hormones).

Then get your serum collected for a total T and SHBG measurement, in the morning just before your next injection. The labs should be available online in 3 days.

You definitely need to find how low your total T is by the next day. If you and your medical professional adviser feel total T is too low, then
either:
a) increase the dosage if you feel (from symptoms) that the maximum dosage isn’t causing you negative issues.
or:
b) increase the frequency if you feel (from symptoms) that the maximum dosage is causing you negative issues.

4) Now introduce your exogenous T, and reduce your HCG, per your medical professional adviser’s protocol, but always keep in mind that the T boost from your reduced doses of HCG will occur for less time than it did when you were doing HCG monotherapy.

2) No one does this

Quickly Determine how fast your body metabolizes HCG, while you’re also supplementing with intramuscular injected T, by:
a) plug a cannula into a vein and sample your blood every 2 hours over 4 days, and get all those samples tested for total T.
then:
b) leave the cannula in the vein and take some HCG, and then sample your blood every 2 hours over 4 days, and get all those samples tested for total T.

Then overlay the T results from the first 4 days, with the T results from the second 4 days, and the difference will be mostly due to HCG (will also include day-to-day variabilities).

3) This method is used by the vast majority:

Take a few years, using trial and error to gradually adjust your HCG dosage and timing, and your intramuscular injected T dosage and timing.

You can sort this out in around only 6 months, if you have a liver which metabolizes hormones very quickly (like mine). Because then the effects of the HCG will occur very quickly, and be obviously noticeable, but they will be gone very quickly, and you will have to inject HCG daily or twice daily.

HCG INJECTIONS – WHEN TO GET BLOOD TESTED

Max T levels will be between 6 to 18 hours after an early morning HCG injection. Fast metabolizers 6 hours (like me) very slow metabolizers 18 hours after.

Usually people notice symptoms of max T from HCG – eg: spontaneous erections, stronger libido. If you’re not noticing those symptoms then most likely your pregnenolone is too low to synthesize enough T from your HCG.

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Get your serum sampled before your morning HCG injection to get lowest T response from your previous day’s dose(s) of HCG.
Get your serum sampled around 6 hours later to see if that’s your peak T.
Get your serum sampled last thing in the afternoon (just before close-of-business for the collection centre) to see if that’s your T peak.

If your T peak occurs over 12 hours after your HCG injection, discuss with your medical professional adviser to conduct a short trial (one or two days) where you inject your HCG just before you go to bed at night.

BENEFITS OF HCG SUPPLEMENTATION

(Drawbacks are explained in the next section)

There are four main benefits of HCG supplementation, three are biological and one is subjective.

Benefit 1: HCG supplementation triggers LH receptors on the leydig cells in the testicles, which resumes testosterone production by those leydig cells.

Without resuming testosterone production, we expose ourselves to the risk of unknown long term complications due to the loss of the manfacture of testosterone precursor hormones which are manufactured by the testicles.

Benefit 2: HCG supplementation triggers FSH receptors on the sertoli cells in the testicles, which resumes sperm production by those sertoli cells.

Without resuming sperm production, we expose ourselves to the being unable to father children via intercourse.

A small minority of males only experience partial testicle size reduction while supplementing with exogenous testosterone without suppementing with HCG. If you’re one of these males, and you’re concerned whether you still need HCG to father children, then discuss with your medical professional adviser to have a semen analysis done to alleviate those fears.

Benefit 3: There may be cells-with-LH-receptors, which trigger actions other than testicular testosterone production by leydig cells.

There may be cells-with-FSH-receptors, which trigger actions other than testicular sperm production.

HCG supplementation will be triggering all LH receptors and all FSH receptors no matter where they are.

Conversely, not supplementing with HCG exposes us to the risk of unknown long term complications due to the as-yet-unquantified loss of LH triggering and FSH triggering in cells other than the leydig cells and sertoli cells in our testicles.

Benefit 4: For those males whose testosterone supplementation also causes testicular shrinkage (the majority, but not all) HCG triggers FSH receptors on the sertoli cells in the testicles, which results in the resumption of sperm manufacture by those sertoli cells, and its those sertoli cells which contribute to the significant majority of the testicle’s size.

Details:

The testicles make several systemic hormones besides T (ie: they make pregnenolone, progesterone, DHEA, androstenediol, and several other less-well-known hormones which we haven’t researched well at all)

The best way to confirm that the testicles contribute to a significant production of several sex hormones, is via analysis of physically (not chemically) castrated (ouch!) males.

Castration is also termed “bilateral orchiectomy”, and this is the term you need to google, eg: “orchiectomy and androstenedione”, then replace the hormone and search again.

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When castration reduces the serum and/or urinary metabolites of hormones, by a measurably significant amount (eg: greater than 20%) then that’s conclusive.

Here are the articles where such analysis was performed:

1) Reduction in androstenedione, androstane, and androsterone after castration.

“Levels of Plasma Steroid Glucuronides in Intact and Castrated Men with Prostatic Cancer”
http://jcem.endojournals.org/cgi/con…tract/62/5/812

NB: since androsterone is manufactured from testosterone by the liver, and since people not supplementing with HCG are still supplementing with exogenous T, therefore people not supplementing with HCG will be manufacturing sufficient androsterone.

and

“Change of serum adrenal androgens in prostatic cancer patients after bilateral orchidectomy or LHRH agonist treatment”
http://www.ncbi.nlm.nih.gov/pubmed/1…?dopt=Abstract

2) Reduction in dehydroepiandrosterone (DHEA) and its sulphate (DHEAS), androstenedione, hydroxyprogesterone after castration

“Orchidectomy or oestrogen treatment in prostatic cancer: effects on serum levels of adrenal androgens and related steroids”
http://www3.interscience.wiley.com/j…76937/abstract

DRAWBACK OF HCG SUPPLEMENTATION
Pituitary Atrophy Of LH and FSH Producing Cells

In all males with a normally functioning HPTA (hypothalamus, pituitary and testicles), their pituitary emits LH from specalized cells call “gonadotrophs”.

This info comes from the following endocrinology online text:

Title: Chapter 3B – Functional Anatomy of the Hypothalamus and Pituitary
Journal: NEUROENDOCRINOLOGY, HYPOTHALAMUS, AND PITUITARY, ASHLEY GROSSMAN, MD – Editor
Authors: Ronald M. Lechan, M.D., Ph.D., and Roberto Toni, M.D., Ph.D.
URL = full text

Here’s the critical excerpt from the above text which describes the “gonadotroph” cells.

Microscopically, the anterior pituitary is composed of nests or cords of cuboidal cells organized near venous sinusoids lined with a fenestrated epithelium into which secretory products from the anterior pituitary are collected. Classically, five cell types and six secretory products of the anterior pituitary gland can be identified immunocytochemically including the somatotrophs (growth hormone), lactotrophs (prolactin), corticotrophs (adrenocorticotropic hormone), thyrotropes (thyroid-stimulating hormone), and gonadotrophs (luteinizing hormone and follicle-stimulating hormone). It is well recognized, however, that the anterior pituitary is vastly more complicated. In addition to morphological and physiological evidence for heterogeneity among the classical anterior pituitary cell types and the presence of clusters of a unique cell type, the folliculostellate cell, the anterior pituitary can also synthesize numerous other nonclassical peptides, growth factors, cytokines, binding proteins and neurotransmitters listed in Table 2 that are important for paracrine and/or autocrine control of anterior pituitary secretion and/or cell proliferation under defined physiological conditions.

__________________________________________________ ________________________________

We need to ask ourselves: Do the pituitary cells which make LH (ie: the “gonadotrophs”) atrophy / degenerate after long term supplementation with exogenous HCG ?

Since only an electron microscope examination of the pituitary is able to observe individual pituitary cells, and their level-of-degradation, therefore we would have to use an electron microscope to inspect the pituitary of a male who has been supplementing with HCG long term, in order to make this determination.

Despite your dreams of male altruism, there are exactly zero males who are supplementing with HCG long term who have made arrangements to have their pituitary inspected after their death, with endocrinology researchers

Therefore the only potential answer to this question comes from rat studies, and here is the only one I’ve ever found:

Title: Morphological changes of pituitary gonadotrophs and thyrotrophs following treatment with LH-RH or TRH in vitro
Journal: Cell and Tissue Research Volume 202, Number 3, 399-406, DOI: 10.1007/BF00220433
Author(s): Masataka Shiino
URL abstract
URL full text (EURO 34)

The researchers removed a 14-day-old rat’s pituitary, and they cultured that pituitary in LH (and TRH too) for 10 days (HCG is structurally very similar to LH, and HCG performs all of the same biological functions as LH, as far as anyone is aware).

The concentrations of LH used in the experiment were much higher than the concentrations of HCG we experience while undergoing male hormone modulation therapy, but the experiment had to be accelerated in order to satisfy the usual budget constraints.

Here’s what the author concluded:

Observed in these glands were external and internal zones, the former containing active, healthy appearing cells, and the latter consisting of many degenerative and necrotic cells

which is obviously less-than-optimum, and…

Hypertrophie gonadotrophs (castration cells) … were observed only in the external zone by electron microscopy. Neither the typical signet-ring gonadotrophs … were seen in the present study.

In other words, the signet-ring gonadotrophs should have been present, but were missing.

The results indicate that LH-RH … alter the morphological features of pituitary target cells

.

In layman’s terms, the rat pituitary cells which are responsible for LH secretion, ie: the “gonadotrophs” (same as in humans) did indeed atrophy – therefore we expect that human pituitary cells responsible for LH secretion (gonadotrophs) will also atrophy as a result of long term HCG usage.

__________________________________________________ ________________________________

The next question we must ask ourselves is:
Can the atrophied pituitary cells which are responsible for LH secretion (gonadotrophs) recover from their atrophied state ?

The longer you supplement with HCG, the longer it takes for your pituitary-cells-responsible-for-LH-secretion (gonadotrophs) to recover, but we’re not yet sure that everyone’s gonadotrophs degenerate to the point where they are unrecoverable.

Eg: Dr Crisler has attempted restarts in young males, and some of them have taken up to 6 months to restart, while a few have never restarted.

But no-one has attempted to restart an aged male who has supplemented with HCG for decades. Certainly endocrinologists have been using HCG monotherapy for over a decade, but no-one is reporting whether any of those initial users have attempted a restart.
__________________________________________________ ________________________________

And the final question we must ask ourselves is:

What’s worse from a biological perspective:

EITHER the known atrophy of pituitary cells which are responsible for LH secretion (gonadotrophs), which may or may not be recoverable,

OR all of the following:
a) the risk of unknown long term complications due to the loss of the manufacture of testosterone precursor hormones which are manufactured by the testicles,
b) the risk of unknown long term complications due to the loss of biological processes which are triggered by LH which occur outside of the testicles, but which have not yet been identified.
c) the loss of motivation from having tiny testicles.

Answer = depends on your perception of risk. I can’t answer that one for you.

WHY SERMS (CLOMID / TAMOXIFEN) SHOULD BE AVOIDED FOR LONG TERM USE

Clomid and Tamoxifen are used in male hormone modulation therapy only as part of a “restart” protocol, as described earlier in this primer.

Any SERM (Clomid, tamoxifen) definitely causes two main problems after long term use:

1) You can’t use any commercially available labs to quantify how your E2 (estadiol) is working in your body. This is because:

…a) SERMS (ie: clomid and tamoxifen) block E2 receptors, so very few of the E2 molecules present in your body will ever be lucky enough to trigger an unblocked receptor. So most of the E2 molecules will simply be “floating junk”.

…b) Measurements of total E2 only measure E2 molecules (which are mostly “floating junk”) but what is actually needed is to measure the number of moecules which get lucky enough to trigger an unblocked receptor.

…c) There are no labs which can measure the “number of trigger events of unblocked E2 receptors”. If we could measure this we would have a direct measurement of E2 metabolism. No such test exists.

2) Long term use of SERMs (ie: clomid and tamoxifen) cause eye issues – especially eye floaters. Google “clomid + floaters”, and “tamoxifen and floaters”, ie:

Google search results for “comid + floaters”

Google search results for “tamoxifen + floaters”

Eye floaters are damaged structures within your eye fluid which appear as visual obstructions to your vision. A floater is identified as a vision obstruction which lags behind a rapid movement of your eye. Ie: if you look up quickly, and the obstruction initially stays where it was and then catches up to where you are looking, then that’s a floater.

The fundamental link between E2 and eye floaters is not well understood, but they accur because E2 levels are too low for too long.

Nor is it well understood why SERMs trigger eye floaters more frequently than aromatase inhibitors such as Arimidex, but that is indeed the case.

SHBG AND DISSOCIATION AND MEGALIN RECEPTORS

T-bound-to-SHBG does indeed dissociate into T and SHBG. The half time for this in vitro is approx 20 seconds.

T-bound-to-albumin does indeed dissociate into T and albumin. The half time for this in vitro is approx 1 second.

The critical info we need to understand is in the competition to provide a free T molecule to bind to an androgen receptor, the free T wins, followed a close second by free-T-which-dissociated-from-T-which-was-bound-to-albumin, and coming dead last by a long long way is free-T-which-dissociated-from-T-which-was-bound-to-SHBG.

Most importantly we use the changes in the ratio of bioavailable T (free T + T-bound-to-albumin) to total T (free T + T-bound-to-albumin + T-bound-to-SHBG) to tell us how our body is processing T, ie:

1) When our body starts changing the ratio of these such that T-bound-to-SHBG is on the rise, then we know our body is trying to downregulate T metabolism (not complete shutdown) by making more T “unavailable for 20 times longer than it was before”

2) When our body starts changing the ratio of these such that T-bound-to-SHBG is being reduced, then we know our body is trying to upregulate T metabolism by making more T “available in 20 times less time than it was before”

We can get an approximate view of these situations simply by monitoring serum total T and serum SHBG.

In other words, the concept of SHBG “prolonging” the life of the T is interesting, but not useful info. What is useful is what we learn from the fact that SHBG is high or low, and that SHBG makes T very much harder to use than when SHBG is lower.

We can indeed treat T-bound-to-SHBG to be as good as useless, compared to the other forms of T.

###

It’s also interesting to note that there are some specific cells which have receptors (the “megalin” receptor) which bind to sex-hormones-bound-to-SHBG, and the sex hormones-bound-to-SHBG do indeed trigger a physiological response (trigger a genetic response once the sex-hormone-bound-to-SHBG enters the cell)

Eg: our liver cells have the majority of our megalin receptors, so that our liver can absorb sex-hormones-bound-to-SHBG so that our liver can metabolize the sex hormones into urinary metabolites.

Statistically the rest of our tissues only have a very low proportion of megalin receptors as compared to their much higher proportion of androgen receptors, and those androgen receptors only bind to free T. Note that T-bound-to-albumin provides free T to androven receptors by dissociating quick enough, but T-bound-to-SHBG dissociates too slowly, so androgen receptors are practically always bound to free T which was recently dissociated from albumin (as part of a T-bound-to-albumin molecule).

Copyright is retained by chilln, 2008, 2009, 2010, 2011

Testosterone Boost 101 (chilln)

johnwester130 · Apr 9, 2017

Many people have been reading about hair loss for years, on immortalhair, on this forum, on hair loss forums, longecity, etc
and honestly no one knows what is causing total baldness.

Shedding can be solved.
Baldness ? - No one really knows.

The best research is focusing on histamine and PGD2.

ddjd · Nov 3, 2018

sladerunner69 said:
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.

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.

jack_zen · Nov 3, 2018

Joeyd said:
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.

which brand and how much adrenal cortex do you take @Joeyd ?

ddjd · Nov 3, 2018

jack_zen said:
which brand and how much adrenal cortex do you take @Joeyd ?

seeking health 50mg. but i hear thorne have a very good product. also it would cause insomnia for someone with already high cortisol levels so watch out.

jack_zen · Nov 4, 2018

Joeyd said:
seeking health 50mg. but i hear thorne have a very good product. also it would cause insomnia for someone with already high cortisol levels so watch out.

only 1 capsule per day?
I am using Swanson which has 350 mg, but don‘t notice too much.
But I have too low afternoon and evenibg cortisol, according to a saliva test

ddjd · Nov 4, 2018

Not perfectly written but an interesting read for anyone who suspects they have low Cortisol and don't respond well to T3

Cortisol

tallglass13 · Nov 4, 2018

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

ddjd · Nov 4, 2018

tallglass13 said:
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

Where did ray say the thing about Pregnenolone boosting cortisol to good levels and then raising Progesterone after??

I think I read a thread from haidut years ago, and listened to a podcast with Danny Roddy where they mocked the idea that Pregnenolone can turn into cortisol. And so I believed them... Might have to do more research.

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