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Messages - Kierkegaard

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1
Injection schedule is daily IM.

Sub-Q is another thing I could try now that weight is down. Sucks to try, transitioning from IM to Sub-Q has sent me into a tailspin in the past.


Wish I could afford Defy, just not possible at this time.

Daily IM?  How much are you injecting?

What about the tailspin when transitioning? 

2
Flyingfool, thanks for your thoughts.

If I go to bed later, I still wake at 3am. There are also these strange states of sleep where I'll awaken at say 2am, then I am kinda asleep but not really.

I am going to raise my dose, hopefully e2 wont run rampant.

What's your injection schedule?

If you do more frequent injections, and also subcutaneous (assuming you're on cypionate/enanthate), you should lower your E2 signficantly.  Otherwise you might consider setting up an appontment with Dr Saya at Defy Medical to get on an aromatase inhibitor. 

3
I have read in multiple places and anecdotally from many folks that low T causes poor sleep. The commonalities and frequency of in particular men stating that when they had low T the woke up between 3 and 4 AM was staggering to me. It not only was poor sleep or sleep disturbances. But the focus on 3-4 AM was very common specifically.

I know that natural T production for men they get a burst of T in the morning. Does anyone know how early in the morning that burst of production takes place?  It would be amazing if that burst occurs at about 3 to 4 AM and may explain why if that burst is too low, that sleep disturbance occurs around that time.

Also at least my experience again anecdotally even whe I was young was “old people” were always extremely early risers. It always seemed odd that when retired and had all the time in the world to sleep in and they are up before the sun. But when young was always hoping to sleep in.  I wonder now if this has to do with the depletion of T with age. And when they wake up due to low T at 4am they simply stay awake!

I know that when younger I had no problems sleeping. Now as my T levels have decreased, I do find myself waking and looking at my clock. And interestingly, it is almost exclusively between 3 and 4 am when I awaken.  Hummmm

Also it seems like many people sleep improves when they get proper hormone levels. This includes thyroid as well as testosterone and I suspect cortisol as well. Cortisol also has a wake response burst or peak early in morning but generally occurs about wake time in the 7-8am or so range.

to me this might be the chicken or egg scenario. I am not sure if low T causes poor sleep or rhe other way. But I suspect it is a negative cycle. Once one gets out of balance, I think the negative spiral build momentum.

My understanding is norepinephrine, cortisol, testosterone, and other hormones (though probably not all of them) peak together at around 6:00 am for the healthy circadian rhythmed person.  The sleep disturbances and especially the early morning awakenings could be a combination of a slightly off-kilter circadian rhythm and the burst of norepinephrine magnified and/or improperly moderated by low testosterone, cortisol, and/or thyroid function, all of which are essential for managing norepinephrine and therefore the entire stress response cycle. 

The 4 am wakings were downright freaky for me.  There was a period for perhaps a year where I would wake and see it still dark out and be like, "okay, this time surely it's at least 5:00 am," and sure enough it was within five minutes of 4:00 am EVERY TIME.

4
When my T got too low when things were really bad, I could only sleep 5-6 hours per night and would wake up like clockwork approximately at 4 am.  TRT took that away, and within a year I tried experimenting by reducing my dose as much as I could and seeing what happened, and when I got too low (something like 20 mg every 4 days), I noticed I was waking up like clockwork at 4 am again.

any possibility it could be related to low e2?

Definitely. 

5
When my T got too low when things were really bad, I could only sleep 5-6 hours per night and would wake up like clockwork approximately at 4 am.  TRT took that away, and within a year I tried experimenting by reducing my dose as much as I could and seeing what happened, and when I got too low (something like 20 mg every 4 days), I noticed I was waking up like clockwork at 4 am again. 

6
I'm not a boozer, but lately since I've been feeling better (thanks to 1500 mg of potassium bicarbonate per day given my barely hypokalemic/low potassium blood levels, as well as 500 mg of phenylalanine, the amino acid that becomes dopamine and norepinephrine) I've been getting more social, and since I'm basically divorced and have lots of free time, I've drank basically more in the last week (two occasions) than I have in the past 4-5 years.

I don't plan on making this a habit.  Nelson Vergel points out how chronic alcohol use can elevate estrogen levels, and I've seen studies to confirm this, such as one that points out that women who consumed over 15 grams of alcohol per day had a 26% elevation in estradiol; other studies I've seen were animal studies and showed similar trends. 

I know the answer is "stop drinking so much," and I plan on doing that if not cutting it out entirely.  The other possibility is that since all the drinks have been beers that my likely sensitivity to gluten has been causing difficulties as well.  I am planning on hanging out soon and will drastically reduce my alcohol intake and try clear liquor like vodka if the urge hits me to try and control for this confound. 

Anyone have experience with this? 

7
Any of the enzymes involved in the adrenal cascade can be affected, as seen by this picture:



The rectangular areas are enzymes.  Because of the feedback loop involved with the hypothalamus-pituitary-adrenal axis, downregulation of any enzyme can have different effects.  The body always has in mind a "set point" for where cortisol should be and will jack up pregnenolone via ACTH (and therefore norepinephrine) to reach this set point. 

For example, in women who have 3B hydroxysteroid dehydrogenase, 21 hydroxylase, or 11B hydroxylase downregulations, you often seen excessive body hair or other masculine secondary sex characteristics.  Why?  Because when one of these enzymes is downregulated/lowered, the body has to pump out *that much more* ACTH/norepinephrine and therefore pregnenolone and other adrenal hormones preceding the downregulated enzyme.  Given that women get half of their testosterone from the adrenals, and higher testosterone goes along with this increased pump out of pregnenolone on down adrenal hormones, you get considerably higher levels of all adrenal hormones before cortisol, including DHEA, androstenedione, and testosterone, the latter two which are "male" hormones. 

So there are different types of symptoms you get depending on the enzymes that are affected.  From the site I just linked on 3B hydroxysteroid dehydogenase enzyme deficiency/downregulation:

"3β-Hydroxysteroid dehydrogenase (3β-HSD) deficiency, due to HSD3B2 gene mutation, is a rare form of CAH characterized by increased levels of pregnenolone, 17-hydroxypregnenolone, and DHEA and decreased levels of all other adrenal steroids (Table 1). Affected individuals usually present in infancy with signs of adrenal insufficiency. Female (XX) infants will typically have mild virilization, and a nonclassic form may appear at adrenarche or at puberty. Phenotypic variation in male (XY) infants may range from hypospadias to complete male pseudohermaphroditism."

This site refers to types of what's called congenital adrenal hyperplasia, and despite the "congenital" term there are two types that aren't congenital and are "acquired".  However, you can have partial downregulations of adrenal enzymes such that you don't qualify for CAH but can still have problems if some of your hormone levels are "on the edge".  Importantly, exogenous testosterone has been shown to slightly reduce enzyme activity of 3B-HSD and possibly (it's been a while since I've looked through the research) one or two other enzymes. 

So if you really want to comprehensively rule out adrenal issues, it's important to get ACTH and cortisol in the same blood draw; the higher the ratio (more ACTH and less cortisol) the more you know that *somewhere* in the adrenal cascade you have an enzyme that's downregulated.  If so, just "backfilling" with pregnenolone doesn't help given how pregnenolone is at the top of the cascade; DHEA often doesn't help either but might (if you have 17 ketosteroid reductase downregulation -- which hasn't been shown to be effected by TRT).  All you can do is take low doses of supplemental hydrocortisone (synthetic cortisol) to correct the ACTH:cortisol imbalance.

So not only does exogenous testosterone (less so with hCG given that the body recognizes it as LH, and not at all with clomid given that it stimulates LH and FSH) cause LH and FSH to drop to zero, leading to less overall pregnenolone and therefore all adrenal hormones; it also slightly (or perhaps in some people moreso) lowers the 3B-HSD enzyme, slightly (or more) unbalancing the ACTH:cortisol ratio in favor of higher ACTH given lower cortisol (which leads via feedback to the hypothalamus to higher accumulation of CRH, and in turn higher ACTH from the pituitary). 

But again, I wouldn't let this worry you if you're on exogenous testosterone; in the vast majority of cases "backfillng" with pregnenolone and DHEA should be more than enough given that most of the effect is with LH and FSH going to zero, not so much 3B-HSD being downregulated -- but again, if you're already low in some adrenal enzymes, exogenous testosterone could put you "over the edge".  If so, it still isn't testosterone by itself that's to blame, but rather your precedent flagging adrenal physiology. 

If anyone wants I can try and dig up more detailed threads on this stuff. 

8
TRT doesn't burn out adrenals.  It tends to slightly downregulate adrenal hormone production because LH and FSH also regulate the conversion of cholesterol into pregnenolone (which converts to other adrenal hormones, including cortisol), leaving all the work on ACTH to stimulate pregnenolone.  Many people don't notice anything, but even if they don't this is why it's recommended to take pregnenolone and DHEA to "backfill" the loss of these hormones when getting on exogenous testosterone.

The dizziness and other feelings you're talking about could be low cortisol, but point more toward low aldosterone (which regulates water retention and therefore blood pressure), but it might be something else entirely.


i have a doubt. what if i scored normal in cortisol but high in urine + acth of 44(considered high) is this from too much stress?

That's a hint that your body has high ACTH and possibly high cortisol (sometimes urine is better than saliva, sometimes not).  If your cortisol is normal, your body is "screaming" ACTH at the adrenals to create enough pregnenolone that becomes a normal level of cortisol, meaning you have a possible downregulated adrenal enzyme.  You more likely are just high in sympathetic activity if we assume high ACTH and high cortisol, which leads to physical and psychological stressors to consider.  Hypothyroidism can cause sympathetic arousal given higher norepinephrine (leading to higher ACTH and therefore adrenals).  Food allergies can be stressors.  But so can boring old psychological stress.  If you've ruled everything you, you might look into adaptogens or phosphatidylserine for cortisol.

9
TRT doesn't burn out adrenals.  It tends to slightly downregulate adrenal hormone production because LH and FSH also regulate the conversion of cholesterol into pregnenolone (which converts to other adrenal hormones, including cortisol), leaving all the work on ACTH to stimulate pregnenolone.  Many people don't notice anything, but even if they don't this is why it's recommended to take pregnenolone and DHEA to "backfill" the loss of these hormones when getting on exogenous testosterone.

The dizziness and other feelings you're talking about could be low cortisol, but point more toward low aldosterone (which regulates water retention and therefore blood pressure), but it might be something else entirely. 

10
If you have hypotension, especially orthostatic hypotension (whether or not it's associated with dysautonomia), you should look into testing aldosterone and renin numbers.  Aldosterone is a water-retaining hormone that works through osmosis via salt regulation.  You can try drinking a glass of water mixed with half a teaspoon of unrefined sea salt. 

11
Curt's death still hasn't sunk in and I suspect it never will given that he was known *as* his words on this forum to so many, and his words will always be here.  So there's no way I'll be able to process Dr C's death.

As a licensed therapist with hundreds of hours working with suicidal clients: please get help.  There are tons of options both psychological and physiological to deal with depression and the alienation that goes with it.

12

The title of the study is: Uptake of reverse T3 in the human choriocarcinoma cell line, JAr.

Wikipedia tells me that Choriocarcinoma is a malignant, trophoblastic cancer, usually of the placenta.

Seems like a stretch to apply this to in vitro normal cells of every other type.

Yeah, I thought the same thing.  But it's better than nothing.  It'd probably be best to lean agnostic on this subject given the dearth of data.
 
Quote
The late Dr. Kenneth Blanchard told me that he was convinced that the reason that many patients did poorly on T4 only meds was the fillers and additives in the different manufacturer's formulations. He said that he saw dramatic differences in patient responses to different T4 only meds.  His favorite T4 med was Tisosint, but after the price of that went through the roof he preferred Levoxyl or Mylan.  Definitely steer clear of anything with povidone in it. After he told me this I actually went through the FDA database and created a spreadsheet with a list of all the inactive ingredients of every FDA approved thyroid medication whether it be T4 only or NDT.

I tried Tirosint, and had the same reaction increasing the dose as I did with Levoxyl and levothyroxine.  I suppose this could be the case with a good number of people, but in my case it seems to go further.  I'm particularly interested in the lowering of cellular respiration that Peat talked about.  Given that mitochondria (which are essential for respiration) and thyroid are mutually reinforcing, there's something to the string of research he's found on the fringes, IMO.

13
Kent Holtorf cites this study in one of his presentations:

The uptake and efflux of reverse triiodothyronine (rT3) in JAr cells were investigated. Uptake of 125I-rT3 was time dependent and reversible with a saturable component of around 70 per cent of total uptake after 30 min of incubation. Efflux was not saturable. Kinetic analysis of the initial specific uptake rates revealed an uptake process with a Michaelis constant of 3.04+/-0.53 microM (mean+/-SEM, n=15) and a corresponding maximum velocity of 9.65+/-2.49 pmol/min/mg protein (n=15). Uptake of rT3 was stereospecific, but not specific for rT3, as unlabelled L stereoisomers of thyroid hormone analogues were more effective as inhibitors of 125I-rT3 uptake than rT3. Unlabelled T3 and thyroxine (T4) (10 microM) reduced cellular uptake of 125I-rT3 by around 82 and 74 per cent, respectively. The calculated inhibition constants Ki were 1.23+/-0.29 microM (n=4) and 0.66+/-0.19 microM (n=4) for T3 and T4, respectively. Similarly, rT3 reduced cellular uptake of 125I-T3 and 125I-T4 by 34 and 23 per cent, respectively. The calculated inhibition constants Ki were 1.75+/-0.55 microM (n=8) and 1.08+/-0.36 microM (n=8) for the inhibition of 125I-T3 and 125I-T4 uptake, respectively. Reverse T3 inhibited efflux of 125I-T3 from the cells by around 20 per cent, but did not inhibit efflux of 125I-T4. These results suggest that uptake of rT3 in JAr cells may occur via a single, saturable membrane carrier, which also interacts with T3 and T4, while efflux of rT3 may occur by passive diffusion.

---

The reason I'm looking for something like this is to explain why some people have bad effects from T4-only medications, such as levothyroxin.  The only other alternatives are pretty obscure references, like Ray Peat, not exactly known for orthodox opinions, who cites a study (though the abstract doesn't reveal this particular statement) in saying that brain slices administered T4 showed a 6% reduction in cellular respiration, which he used as evidence that T4 without the proper ability to convert to T3 (i.e., poor liver function, ironically part of the hypothyroid picture for many patients) causes more harm than good.

As excellent a researcher as Peat is, nowhere does he say that rT3 inhibits cellular uptake of thyroid hormone, T3 or T4.

Thoughts?

14
Testosterone, Hormones and General Men's Health / Re: 1000 mg of Vitamin C
« on: September 17, 2018, 01:05:30 pm »
I'd just be cautious about approaching 2 grams a day because is the upper tolerable limit per the excellent Pauling article Cataceous linked.

15
Testosterone, Hormones and General Men's Health / Re: 1000 mg of Vitamin C
« on: September 16, 2018, 05:53:17 pm »
Dr Jonathan Wright notes that primates like ourselves that lack the enzyme that allows us to make vitamin C -- meaning it's an essential vitamin -- consume about 3 grams of vitamin C daily, and thinks we should approximate the same.  He's big time into Linus Pauling's work, and holds that we should consume vitamin C to the point of bowel tolerance: once our stools become loose or we get other digestive issues, go back to the previous dose after building up.

Of course, this is far from the conventional stance, which doesn't even consider vitamin C worth supplementing except maybe when we're sick.  YMMV.  One slight concern is that vitamin C is a cofactor for the enzyme that converts dopamine to norepinephrine, so if you're low in the former and high in the latter you might reconsider C supplementation.  But at the same time, vitamin C seems to be almost an adaptogen with regard to its ability to help the adrenals.  Even Dr Jefferies, in his epic Safe Uses of Cortisol, considers it for this reason. 

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