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Messages - Simeoni

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1
JBone if you decide choose the AI route, please give us an update how it works out for you.

Good luck!

2
Well I can only say that for me a peak of 1200 ng/dl is too much. Now im sure there are many who do not have  a problem with this - meaning they dont get too much cortisol suppression.

Are you able to try more frequent injection protocol - like every other day? That could balance both ends of the scale so you dont get too much cortisol supression.

Regarding the increase in ACTH - and thus cortisol -  I think that the effects should come about pretty fast. For me I saw an noticeable increase in my cortisol levels in a matter of two weeks.

During the first weeks the side effects were also stronger and they eventually lessened as the treatment continued. There seems to be many who quit this treatment during the first weeks. So if you decide to try this route I suggest you stay on the treatment for at least 6-8 weeks.

For me the use of HCG is not a must but it does have enough benefits to take it regularly.

Regarding morning a healthy morning cortisol levels here is a quote from dr Mariano:

"A person at rest who is un-stressed (e.g. hasn't lifted weights the day before) generally will have a morning cortisol level of between 17-20 ug/dL. If stressed, the cortisol should be higher. This means the person has mounted an adaptive response to the stress to stay healthy and functional. For example, if a person lifts heavy weights the day before, the stress of this may raise the morning cortisol to around 30 ug/dL. This may be "elevated". But it is a normal healthy state. Thus interpreting cortisol also means taking into account the stresses a person is experiencing.

If cortisol becomes substantially lower than 17 ug/dL, then that person is failing to adapt to stress. And past a certain level, that person will become frankly ill. Examples of this state includes posttraumatic stress disorder. Addison's disease is a condition where one is unable to make cortisol due to damage to the adrenal glands. In PTSD, the problem is not the adrenal glands. The problem is that the brain is unable to produce sufficient ACTH in response to stress (norepinephrine signaling). This results in insufficient cortisol to respond to the stress to keep a person healthy and functional.

The failure to produce sufficient Cortisol means one is unable to reduce norepinephrine signaling in response to stress - Cortisol's most important function. One cannot immediately calm oneself down in response to stress. The other adrenal hormones are released along with Cortisol. This means they too would be at deficit. Progesterone and Testosterone for example are calming to the nervous system. Mood then becomes unstable as norepinephrine stimulates the negative subcortical emotional systems of FEAR, RAGE, and PANIC-GRIEF. In children, you see them having tantrums. In adults, you may get anger outbursts or panic attacks, among its many manifestations. Failure to produce sufficient Cortisol also means inflammatory signaling is not controlled. As inflammatory signaling goes up, energy production is shut down, depressive syndromes occur, etc.""

Now my cortisol tests have mainly been in the nmol/l range and I see 450-550 nmol/l as a healthy level for me. So I would say that having morning cortisol at the upper end - not over the range - is an indicator of a healthy HPA-axis.

I have also been suffering with low HPA-Axis activity in the past so I want to offer my own experiences.

I know that doctor Mariano has used low dose SSRI to treat the hypoactivity of the HPA-axis. At least he has done this in the past. Im not sure what is he's stance today.

Here is an excellent write up on how low dose SSRI might help with low cortisol:

http://corpus-scientia.com/forum/index.php?/topic/161-ssris-inhibit-cortisol-negative-feedback-in-humans/

I have tried this route myself and I do feel that it works. For me the most important thing was to keep the dose low enough so that you avoid the unwanted side effects.

I was using 2,5mg of escitalopram for over a year and at some point I just felt that I did not need it anymore. I did a slow taper and noticed that my cortisol stayed in good range even without the SSRI. Other thing that made me want to stop it  was the emotional numbing that SSRI's often cause.

Other things that I have tried are nicotine patches which improve the activity of the HPA-axis by increasing the release of ACTH from the pituary gland. For me this route is more of an first aid than a long term treatment option. But I do feel that it works. The idea is to use the patches is small portions. For example if you have a patch which has 24mg of nicotine - released in a period of 24 hours - you can cut the patch in quarters and take one quarter a day.

At the moment nicotine patches are more of an nootropic for me than a way to increase cortisol.

Other things that have been a big factor for me are:

1. Sleep

- If I dont sleep enough it will eventually lead to a lowered cortisol output. So good sleep hygiene is a must for me

2. Keeping my testosterone dose low enough

- If I go too much past the  1000 ng/dl mark of total testosterone, that will eventually lead to low cortisol also. Keeping the dose low enough and using a EOD injection protocol has worked great.

3. Using HCG

There are anecdotals where people have reported that using hcg with test injections has improved their cortisol levels. I cannot say for certain that this has been the case for me.

4. Thyroid hormones

if you are hypo that can  eventually lead to low cortisol levels. So having a healthy levels of thyroid hormones may increase ACTH output. Here's one study that showed just that: https://www.ncbi.nlm.nih.gov/pubmed/2553572

Now I have also tried pregnenolone in the past but I cant say - without labs - that it helped with low cortisol. I do think it improved my sleep a bit.



Thank you for such a great in-depth response!

What would you think if a person's TRT dosage puts them at around 1200 for a day or so and by the end of the week they are around 500-600, is that too much and will cause cortisol suppression?

How long does it take to notice they effects of the low dose SSri? Did you experience any side effects at the beginning of the SSri treatment?

Would you say Hcg is a must if on TRT?

With your current knowledge what would you say is a good morning serum cortisol level?

3
I have also been suffering with low HPA-Axis activity in the past so I want to offer my own experiences.

I know that doctor Mariano has used low dose SSRI to treat the hypoactivity of the HPA-axis. At least he has done this in the past. Im not sure what is he's stance today.

Here is an excellent write up on how low dose SSRI might help with low cortisol:

http://corpus-scientia.com/forum/index.php?/topic/161-ssris-inhibit-cortisol-negative-feedback-in-humans/

I have tried this route myself and I do feel that it works. For me the most important thing was to keep the dose low enough so that you avoid the unwanted side effects.

I was using 2,5mg of escitalopram for over a year and at some point I just felt that I did not need it anymore. I did a slow taper and noticed that my cortisol stayed in good range even without the SSRI. Other thing that made me want to stop it  was the emotional numbing that SSRI's often cause.

Other things that I have tried are nicotine patches which improve the activity of the HPA-axis by increasing the release of ACTH from the pituary gland. For me this route is more of an first aid than a long term treatment option. But I do feel that it works. The idea is to use the patches is small portions. For example if you have a patch which has 24mg of nicotine - released in a period of 24 hours - you can cut the patch in quarters and take one quarter a day.

At the moment nicotine patches are more of an nootropic for me than a way to increase cortisol.

Other things that have been a big factor for me are:

1. Sleep

- If I dont sleep enough it will eventually lead to a lowered cortisol output. So good sleep hygiene is a must for me

2. Keeping my testosterone dose low enough

- If I go too much past the  1000 ng/dl mark of total testosterone, that will eventually lead to low cortisol also. Keeping the dose low enough and using a EOD injection protocol has worked great.

3. Using HCG

There are anecdotals where people have reported that using hcg with test injections has improved their cortisol levels. I cannot say for certain that this has been the case for me.

4. Thyroid hormones

if you are hypo that can  eventually lead to low cortisol levels. So having a healthy levels of thyroid hormones may increase ACTH output. Here's one study that showed just that: https://www.ncbi.nlm.nih.gov/pubmed/2553572

Now I have also tried pregnenolone in the past but I cant say - without labs - that it helped with low cortisol. I do think it improved my sleep a bit.

4
Could you post all your thyroid labs that you have taken? I do not think that your E2 is high enough to warrant all those symptoms.

5
Your serum levels should bounce back in a matter of 1-2 weeks. From what Ive seen the low e2 symptoms might linger on a bit longer. Everyone is different but it might take as long as 4-8 weeks.

I suggest you keep your dose steady and do not take any drastic measures - like reintroducing an ai - without pulling labs first.

Im not 100 percent sure yet but I'm fairly certain I took too much arimidex and crashed my E2.  I will be getting bloodwork on Thursday to confirm.

 So I've been under a lot of stress lately and I think I accidentally took too much arimidex.  I haven't felt this awful since before I started trt.   I've never experienced brain fog like this. Feels like I have not slept in days even though I'm sleeping through the night. And I have a twitch in my  left eye which is driving me absolutely crazy.

 Just wondering in the event that it is a crash of  E2, is there anything I can do to recover more quickly?

 What kind of timeline am I looking at to bounce back?

6
Sad to hear this! I always saw him as a warm and humble spirit.

There never was anything mean or ego driven in his writings. He was a good example on how to create a truly helpful community!


7
That's pretty interesting.

If I have understood correctly it has at least been shown that the prolonged use of AAS upregulates the AR - in the muscle tissue. I wonder if dopamine plays a bigger part in this.

The constant increase in dopamine signaling - that's caused by high amounts of testosterone - can't be good in the long run. DR desensitizes eventually.

8
In my opinion your estradiol is low enough to warrant many of your symptoms. 52 pmol/l translates to 14 pg/ml. Also since it was not the sensitive assay it could be even lower.

Have you used any form of AI?

9
So what's the recommended dose nowadays?

The last time I followed the the iodine conversation there seemed to be two camps in regards to dosing - the ones promoting taking it in the mg's and others mcg's.

When I did my last trial with iodine I choose to take it in the micrograms.

11
Testosterone, Hormones and General Men's Health / Re: Sustanon dose
« on: December 13, 2017, 03:14:32 pm »
If by 1/2 tablet of arimidex every day you mean 0,5mg, then thats way too much. You will crash your estrogen fast and feel miserable for a long time.

Start with a much lower dose and move from there.

12
In my understanding anything that increases your net opioid tone will also improve mood. I also tried LDN for a while few years ago. Felt pretty good for the first week. Then the positive effects vaned and I started to get low cortisol symptoms.

Thi seems to be the experience for many. I would keep an eye on your HPA axis functioning if you plan to use it for a longer period.

13
I went through again the study that Jay posted. He said that

"Last sentence:
Thus, it appears that the
decline in E, sensitivity which follows ovariectomy cannot be attributed
to a decrease in the number of POA-MBH estrogen receptors capable
of translocating into the cell nucleus, but is more probably associated
with a change in the processes subsequent to ER, binding.
"

That was not actually what the study said. The direct quote says that: "Thus, it appears that the decline in behavioral responsiveness to E2 which occurs after ovariectomy cannot be attributed to a decrease in the ability of E2 to translocate estrogen receptors into POA-MBH cell nuclei, but is more probably associated with a change in the biochemical processes subsequent to ERn binding."

Loss of behavioral response to E2 is not the same as E2 receptor desensitization. It's possible that this change in behavior was brought by some other effect that the E2 deprivation had on the rat brain. I do not feel that you can use this study as a proof to your theory.

I dont want to put you on the spotlight with this, but I do feel that its important be thorough when using studies to back up our theories.


14
Shbg levels are never static. The drop from 26 to 22 falls in the range of normal variation. Its nothing drastic in my opinion.

Now in my case I used to always have my shbg in the 39-49 range. After increasing my DHT, I now seem to have it in the 25-29 range. I have confirmed this with multiple blood draws.

15
I have gone through the same ordeal so I can relate to this topic. I want to comment on one thing that was mentioned in this thread.

JayDoe brought up to idea that estrogen deprivation might lead to receptor desensitization. Jay also brought up studies in a attempt to back this up. My question is: where does the study talk about receptor desensitization? Here's the link: https://www.sciencedirect.com/science/article/pii/0018506X81900180?via%3Dihub

It does talk about the reduction in progesterone receptors but not estrogen: "However, no differences were observed between long- and short-term OVX rats with respect to ERn concentrations"


One thing's that the studies do show is the effects of estrogen as a neuroprotective agent. The loss of a certain amount of dopamine producing neurons was observed in a one study done in OVX female monkey's ( https://www.sciencedaily.com/releases/2000/12/001204072446.htm ).

Summary on that study would seem to show a:

- 30% loss of dopamine producing nerve cells in the substantia nigra - which plays a big role in motivation, reward and movement.
- low/depraved state in that study was an E2 level below 15 pg/ml - and it was not the sensitive assay.
- those with short term deprivation (10days) seemed to recover the lost neurons with a brief E2 treatment.
- those with long term deprivation (30 days) did not recover the lost neurons.

Few caveat's and why we should not think that this study directly correlates with humans:

- Looking at the full study we see that the mentioned "brief" estrogen therapy meant 2 days. That is a very short duration and I would assume that the other group would have seen some recovery with a longer time of estrogen therapy.
- There are hundreds of people and anecdotes in different forums who have gone through a long state of very low estrogen. If that would mean permanent loss of your dopamine producing neurons, I think that we would see a lot more of "fuss" about it - like we see with pfs syndrome.

That said. I do think that its safe to say that estrogen is important in protecting your dopamine producing neurons. I can also relate to the experience where you feel awful for a long time after a crash - even tough your e2 is within range. I was in a dark place for months. My symptoms did resemble those of low dopamine function: poor drive/motivation, low libido, cant enjoy anything etc.


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