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Topics - Kierkegaard

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Testosterone, Hormones and General Men's Health / Anastrozole Lozenge?
« on: March 29, 2017, 09:44:19 pm »
How hard are these to compound or find a doc who's willing to compound them?  I'm thinking of asking my doc for one to bring my E2 down a few points -- CDG could be helping, but not enough, and for whatever reason my E2 shoots up 5-10 points during allergy season (perhaps caused by histamine).

Something that seems to have been happening in the last year or so while being on 26-30 mg subq cypionate E3D is that I'll feel higher estrogen symptoms the last day or so before my injection; the first few years being on TRT I'd feel them as I approached my peak at 30 hours or so. 

My speculation is this is estradiol hanging around while T levels are dropping -- something Dr Mariano and others have told me happens in their experience.  Right now I've hit too-high E2 levels, although this is complicated because this seems to happen during allergy season for me (March through May), which kicks up E2 by 6-10 points.  I'm thinking of going EOD again to see if this cuts my E2 level relative to T. 

Anyone else experience this "estradiol floating through as T drops" effect?

Simple question.  I'm wondering if the depot (hard knot that sometimes happens with subq injections of cypionate) could allow for less absorption.  Any thoughts?

Although basically medical word vomit, this is still a very interesting and potentially very useful resource for people seeking non-pharmacological methods to lower E2.  Turns out quercetin, which I've been using and noticing lower estrogen effects, actually is considered a small-moderate AI.  The conclusion of the article (and there's plenty more in other places, so check there):

    Nearly 300 natural product compounds have been evaluated for their ability to inhibit aromatase, in noncellular, cell-based, and in vivo aromatase inhibition assays. Flavonoids have been tested most frequently and generally found to be the most active class of natural product AI compounds. Some of the more active flavonoids included apigenin (8 ), chrysin (11), 7-hydroxyflavone (26), isolicoflavonol (27), (2S)-abyssinone II (45), (2S)-2',4'-dihydroxy-2-(1-hydroxy-1-methylethyl)dihydrofuro[2,3-h]flavanone (49), eriodictyol (50), 8-prenylnaringenin (62), 3'-[γ-hydroxymethyl-(E)-γ-methylallyl]-2,4,2',4'-tetrahydroxychalcone 11'-O-coumarate (75), isoliquiritigenin (77), and rotenone (132). Other very active AI compounds included the xanthone, γ-mangostin (239), the sesquiterpene lactone, 11βH,13-dihydro-10-epi-8-deoxycumambrin (211), and the anthraquinone, benzanthraquinone I (249).


(From his post on reddit):

I claim that excessive reduction in inflammation can cause insomnia. This means a summation of signals that leads to excessively low pro-inflammatory signaling impairs sleep.

In my opinion, inflammatory cytokines are the most important signals for sleep.
When you are ill from an infection such as the flu or Hepatitis C, etc. they strongly trigger sleep. It is a primary reason exercise and physical activity in the daytime are strong behavioral interventions to help sleep. Physical activity increases proinflammatory cytokine signaling which then promotes sleep. In mania - where a person may not sleep at all for weeks - there is not enough proinflammatory signaling to balance the excessive norepinephrine signaling that leads to mania. Mood stabilizers reduce both norepinephrine and pro-inflammatory cytokine signaling. Prednisone at a sufficient dose can trigger mania by reducing inflammation excessively.

I arrived at that conclusion through understanding the physiologic mechanisms underlying sleep through multiple texts and articles on psychoneuroimmunology, endocrinology, immunology, neurology, psychiatry, psychology, neuroscience and sleep science, along with 30+ of study and clinical experience and observations of thousands of patient responses to treatment. As a physician, that has significant weight.

By "stress hormones" which do you mean?

If you mean norepinephrine, then realize that it is the primary signal of the sympathetic nervous system when it is activated by other brain cells, the immune system, or other cells in the body. The adrenal medulla which systemically releases norepinephrine (and epinephrine, its daughter molecule) is essentially a ganglion of the sympathetic nervous system.

If you mean proinflammatory cytokines from cells of the immune system and other cells such as glial cells and fat cells, then yes, proinflammatory cytokines activate the sympathetic nervous system in general. But the triggering of the anti-stress and anti-inflammatory hormones of the adrenal cortex by the sympathetic nervous system can rapidly quell the sympathetic nervous system activation. In a generally healthy person, the nervous system automatically calms itself down and quells inflammation systemically by triggering adrenal cortex hormone signaling. The loss of this signaling cascade results in uncontrolled stress and inflammatory signals that lead to numerous illnesses (e.g. depression, diabetes, obesity, heart disease, hypertension, anxiety, cognitive dysfunction, etc. etc). Proinflammatory cytokines also can have anti-inflammatory effects depending on the circumstance and the summation of signaling from every cell involved.

Many think that adrenal cortex hormones are "stress hormones". They are not. To think so is a misreading of the literature. They are anti-stress and anti-inflammatory hormones. They calm both the stress system (which has norepinephrine as the primary stress signal) and the immune system (which have the proinflammatory cytokines as the primary stress signals).

Again, the summation of signaling is important. For example, estradiol has both anti-inflammatory and anti-stress functions but it can also be inflammatory and can cause stress - depending on the location of action and circumstance and the mechanism involved - of which estradiol has over 400 mechanisms of action. For example, some patients develop panic attacks or rage when estradiol is excessive for them. And some patients are calmer and are able to sleep better, and have fewer hot flashes, when estradiol is improved from a deficit. Estradiol is needed to reduce joint inflammation - having a role in connective tissue formation. But it can also increase the release of hepatic C-reactive protein - an inflammatory signal associated with a higher risk of heart disease. These actions depend on multiple signaling interactions but one has to keep them in mind when assessing a patient.


Also a great point on how TMG (i.e., Betaine) is much more useful than for digestive issues:

Betaine or Trimethylglycine provides:

Three methyl groups. These can be used to create SAMe from Homocysteine. SAMe then acts as a cofactor for COMT which gets rid of excess norepinephrine. Norepinephrine is the primary signal that keeps you awake.

Glycine. Glycine is an inhibitory (i.e. sedating) neurotransmitter like GABA. Glycine also unlike GABA improves memory by preloading the Glutamate Receptor for activation. Glycine alone can be used to improve sleep.

SAMe also is a cofactor in producing certain neurotransmitters including serotonin. Serotonin is a calming neurotransmitter - helping reduce norepinephrine signaling. Serotonin can also be converted to Melatonin, which helps sleep.


Also worth noting that he told me on the phone that Betaine HCL *is not* used primarily to produce acid in the stomach, and I forgot to ask him if pepsin is the real ingredient, which I assume would have to be the case. 

I find claims like this that seem to support it: "A woman's menstrual cycle can also affect vision. "During the first week of menstruation the typical elevated estrogen level can cause blurred vision, trouble focusing, and watery eyes," said Dr. Kondrot." (from a simple google search)

This is something that seems to go with me having highish estrogen/E2/E2 metabolites.  Anyone else?

After a few months of being off DIM because iodine seemed to provide much of the estrogen support provided by DIM, and also being on 12.5 mg of iodine, lowering my dose because at slightly higher doses I got back an iodine loading test and revealed 80% saturation of iodine (you can usually lower your iodine dose as you take it to retain the same level of saturation), it seems like reintroducing 50 mg of DIM (100 mg DIM-Plus) is likely causing my blood sugar to go too low.

It started with moderate hypglycemia episodes (I've only gotten them once before when I was sick with a cold), involving anxiety, slight shakiness, hunger, and sometimes slight lightheadedness/brain fog, and I checked my daytime glucose and it came back in the 70s two different times and tonight at 60 -- all three times the lowest it's ever been.  I also checked fasting glucose and it was also in the 70s. 

Given that I was previously on 75 mg DIM when I started upping my iodine (which apparently takes a while to saturate tissues) and never had this problem, with glucose levels sometimes approaching prediabetic levels, it seems like being on iodine longterm has helped lower my glucose, and adding DIM after being on iodine for months without being on DIM has put me over the edge.

This could actually be a very good thing.  Dr Fletchas, one of the iodine experts has written about high-dose iodine's glucose-lowering effects and less need for insulin with type two diabetics:

  • It was while treating a large 320-pound woman with insulin dependent diabetes that we learned a valuable lesson regarding the role of iodine in hormone receptor function. This woman had come in via the emergency room with a very high random blood sugar of 1,380 mg/dl. She was then started on insulin during her hospitalization and was instructed on the use of a home glucometer. She was to use her glucometer two times per day. Two weeks later on her return office visit for a checkup of her insulin dependent diabetes she was informed that during her hospital physical examination she was noted to have FBD. She was recommended to start on 50 mg of iodine(4 tablets) at that time. One week later she called us requesting to lower the level of insulin due to having problems with hypoglycemia. She was told to continue to drop her insulin levels as long as she was experiencing hypoglycemia and to monitor her blood sugars carefully with her glucometer. Four weeks later during an office visit her glucometer was downloaded to my office computer, which showed her to have an average random blood sugar of 98. I praised the patient for her diligent efforts to control her diet and her good work at keeping her sugars under control with the insulin. She then informed me that she had come off her insulin three weeks earlier and had not been taking any medications to lower her blood sugar. When asked what she felt the big change was, she felt that her diabetes was under better control due to the use of iodine. Two years later and 70 pounds lighter this patient continues to have excellent glucose control on iodine 50 mg per day. We since have done a study of twelve diabetics and in six cases we were able to wean all of these patients off of medications for their diabetes and were able to maintain a hemoglobin A1C of less than 5.8 with the average random blood sugar of less than 100. To this date these patients continue to have excellent control of their Type II diabetes. The range of daily iodine intake was from 50 mg to 100 mg per day. All diabetic patients were able to lower the total amount of medications necessary to control their diabetes. Two of the twelve patients were controlled with the use of iodine plus one medication. Two patients have control of diabetes with iodine plus two medications. One patient had control of her diabetes with three medications plus iodine 50 mg. The one insulin dependent diabetic was able to reduce the intake of Lantus insulin from 98 units to 44 units per day within a period of a few weeks.

Yeah, he doesn't provide a reference for his study, but this "at the office" study is definitely something to consider. 

Regarding DIM, it's recommended to be cautious if you have diabetes:

    DIM may affect blood sugar levels. Caution is advised in people with diabetes or hypoglycemia, and in those taking drugs, herbs, or supplements that affect blood sugar. Blood glucose levels may need to be monitored by a qualified healthcare professional, including a pharmacist, and medication adjustments may be necessary.

So my working hypothesis is that DIM and iodine independently lower blood sugar, perhaps have an interaction effect (i.e., both together causing more lowering than either independently added together), and will try getting off DIM in the next few days and see how my glucose looks. 

Only bummer is I haven't been checking glucose in the last few weeks since being on 12.5-18 mg of iodine.  Will keep you guys updated. 

I'm speaking of the claim that transdermal progesterone can get "caught" in a guy's fat and stay there for weeks if not longer.  Any solid argument for this?

I've said it a few times here that the fact that doctors use corticosteroid shots to stop panic attacks proves the power of cortisol as an "antistress hormone" in the words of maybe the world's greatest endocrinologist, Thierry Hertoghe.  This post from another forum shows you how hydrocortisone (in combination with thyroid hormone) can dramatically lower anxiety.

  • Throughout the 80s, 90s and early 2000 I used to have the most frightening panic attacks that appeared to come out of nowhere. As time went on they would wake me up and one of the most common times it would happen towards the end was when out walking with my dog. I remember staggering like a drunk with my heart pounding, pouring with sweat and legs that wouldn't work. I wouldn't wish it on anybody.

    However since taking a cortisol replacement from late 2002 to date and also thyroid replacement I am delighted and more than relieved to say that I have never had a panic attack and never felt like I would. I have zero anxiety these days (I used to be extremely anxious but never knew why) so the issue of low cortisol and possibly a knock on with low thyroid is an often overlooked cause of anxiety and panic attacks. It's all a distant memory for me but one I will never forget and I feel for anybody who is going through this now.


I haven't gotten around to testing my E2 since going from E3D to EOD, but I'm having pretty intense fatigue and hypersomnia, sleeping sometimes 12 hours feeling less rested than when things were more aligned in the past and I could sleep 8.  I'm also not having clear high E2 symptoms.  I went from my usual 28 mg E3D to currently 20 EOD.  I know, per Saya and others, that injecting more frequently with the same amount means higher levels of T and therefore E2, but I also know that going from every 3 days to every other day theoretically should mean a pretty significant drop in E2.

Anyone have any experience with E2 dropping pretty significantly going from E3D to EOD or daily, etc.?

So it seems like there are many roads that lead to Rome.

DIM works through changing estradiol metabolites, particularly in speeding up 2- and 4-hydroxyestrone pathways (possibly not the latter according to at least one study I've seen), which would mean less 16a-hydroxyestrone (bad estrogen) as the other pathways are moving faster draining more estrogen away from it. 

Indole-3-carbinol, the daddy of DIM from which DIM is a metabolite, apparently does the same but lowers 4-hydroxyestrone (a good thing, as this is a "bad" estrogen), at least according to one study I've found.

Iodine (in relatively high doses of 1-3 mg according to Jonathan Wright, and Dr Brownstein recommends doses ranging from 12 to 50 mg for many patients, but only when working with an iodine-savvy doctor) reduces estradiol in favor of estriol and therefore theoretically lowers 16a-hydroxyestrone, which is an intermediary step between estradiol and estriol (according to Wright).   

Aromatase inhibitors slow down the aromatase enzyme, allowing for less conversion of testosterone to estradiol (but does nothing to the estradiol metabolites mentioned above).  Zinc can be considered an aromatase inhibitor and is used in lieu of anastrozole by Dr Mark Gordon.  But make sure you watch your copper and ceruloplasmin levels, as zinc and copper oppose one another, so it's good to supplement with copper if you're going the zinc route. 

You can also lower estradiol in a probably safer way without supplements by injecting more frequently and/or injecting subcutaneously (which likely decreases the peak of testosterone and therefore E2 as well).

And CDG clears out estrogen via inhibiting betaglucuronidase (whatever dat is) and also apparently lowers the number of estrogen receptors (meaning it's sorta like clomid, which binds to estrogen receptors rather than reduces their number). 

Of course the American tendency is to say "hey, I've got high estrogen!  So I bet trying ALL these supplements could REALLY help."  Not recommended! 

And this stuff is pretty complicated, because there are so many different things going on here: reductions in estradiol, reductions in estradiol receptors, reductions in 2-, 4-, and 16a-hydroxyestrone, and each of these changes in variables can have associated symptom changes as well as influences on things like cancer rates. 

It's like the body is complicated or something. 

Just found out my wife's grandfather was diagnosed with prostate cancer -- BUT it's either at the earliest possible stages or in a pre-cancer stage, because nobody is worried about anything.  He wants to try natural routes before getting on medication, which was offered by the doc but my wife didn't mention which -- probably finasteride or something like it that blocks 5a-reductase and so reduces the conversion of testosterone to DHT.

Being a small town doctor he goes to, the doc is almost certainly into the idea that DHT and not estradiol is the main culprit in prostate cancer.  My wife's gpa is into trying natural alternatives instead, so the first thing that comes to mind is anything that blocks 4-hydroxyestrone (a main "bad" metabolite of estradiol; see my rambling DIM sticky thread for pictures), and I know this contributes to prostate cancer specifically, given that I have the homozygous polymorphism that codes for the enzyme that converts estradiol to 4-OHE, and this has been proven to have a one-third reduction in risk of developing prostate cancer.  As I rambled on in my thread above, the research is at the most contradictory as to whether DIM *stimulates* this same enzyme, and indole-3-carbinol, from which DIM is a metabolite, apparently *inhibits* this enzyme while also stimulating the 2-hydroxyestrone pathway. 

So I'm thinking of recommending I3C to him.  The tricky thing here is he's not going to be going out of the mainstream medical establishment, so I can't say things like "with your doctor's supervision."  But he's not going to be trying the medication offered to him.  Another option is to have his estradiol and total T pulled, even if he has to drop cash on his own to get it, to see where he's at for a T:E2 ratio.  Then it's up to suggesting zinc, calcium d glucarate (tough he's pushing mid-80s, so increases in calcium are probably not good), and other E2 lowering supplements. 


Effects of short-term supplementation with ascorbate, folate, and vitamins B6 and B12 on inflammatory factors and estrogen levels in obese postmenopausal women.

  • Abstract
    Little is known about the effects of commonly used vitamins on serum inflammatory markers and the hormonal balance in obese postmenopausal women. We studied the effects of an 8-week open-label supplementation with vitamins C (500 mg), B6 (25 mg), B12 (1 mg), and folate (5 mg) on C-reactive protein, interleukin-6, and estradiol levels in 20 obese (body mass index > or = 30) postmenopausal women. Outcomes were assessed in a blinded fashion. Folate and vitamin B12 levels rose significantly, suggesting that the supplement was well absorbed and that participants adhered to the protocol. Weight, blood pressure, and serum lipids remained stable. C-reactive protein, interleukin-6, and leptin levels remained unchanged. Estradiol levels rose from a median of 22.0 pg/mL (IQR = 15.9-25.8) at baseline to a median of 27.8 pg/mL (IQR = 23.1-33.9) at follow-up (p = 0.003). Increments in serum estradiol caused by vitamin supplementation in postmenopausal women have not been previously described and probably merit further investigation.

Man, there's no such thing as a nutritional free lunch, is there?  Which harkens me back to the mistake of following my old doctor's advice and trying 4 mg of methylfolate, literally 10 times the RDA (close to the 5 mg in the study) and with the extra kick of being "activated" via methylation to boot, and me having what probably were terrible high estrogen symptoms at the time. 

So if you have to take high doses of folate and B12 for whatever reason, perhaps you should consider adding calcium d glucarate to the mix to keep estradiol levels stable. 

Extra: high-dose B6 (200-800 mg/day) lowers estrogen and raises progesterone

Yikes, guys.  I didn't think this iodine stuff was helping that much until I decided to drop from 25 mg to 12.5 mg as an experiment (more on this below).  I'm coming off a three hour low-grade anxiety period (not an attack) with slight palpitations, bloating, fluid retention, and a massive appetite, BUT a pretty powerful sex drive with good erections.  A year ago and before I'd have all these at once with less intensity (except for the sex drive and libido) for about an hour but (strangely) also get really (nicely) sleepy and end up taking a nap around my peak at 36 hours, which usually meant a nap right after work. 

The experiment part involved trying to get off DIM completely (which I have been for over a month) to see if iodine can replace DIM in terms of its estrogen metabolism changing effects.  I cut the dose in half after taking a day off to take the iodine loading test (where I needed to not take iodine for 48 hours, then ingest 50 mg of iodine, then collect urine for 24 hours, all to see how high my flouride, bromide, and iodine levels are) and noticed I felt better, and also from noticing that I seemed to have pushed through my sweet spot by taking too much iodine.  So it looks like I'll be returning to my 25 mg dose minus one drop of Lugol's 2% worth (2.5 mg iodine) tomorrow. 

Just a reminder that iodine, according to the unpublished (to my knowledge) research of a very research-friendly doc, Jonathan Wright, changes estrogen metabolism by likely draining away 16a-hydroxyestrone, leading to reductions in estradiol and/or increases in estriol.  16a-OHE is one of the main carcinogenic estrogens, the other being 4-hydroxyestrone, which is another metabolite with estradiol.  The DIM that I was on apparently increases 2-hydroxyestrone (good) but likely (still some contradictory research) 4-hydroxyestrone as well (bad; more info on my thread here).  You can think of these three estrogen metabolites as drains for estradiol, but a good number of guys don't seem to notice a significant drop in estradiol (i.e., not accounted for by lab error) by taking DIM, and this is because DIM increases aromatase -- and yet a lot of guys (including myself) feel better on it! 

FWIW, I just got lab results back for estradiol since being on 25 mg iodine for a few months and also being off DIM, and my E2 went down from around 34 to around 24 pg/ml compared to before getting on iodine and being on 75 mg DIM.  HowEVER, at the time of this lab draw I was experiencing what seems like low estradiol symptoms (increased fatigue, clay-colored stools, poor erections and libido), which previously with DIM at levels of 24 pg/ml I wasn't experiencing.  So this could mean that iodine, by changing how estradiol is metabolized (toward estriol thereby draining 16a-OHE) compared to DIM (higher 2-OHE and 4-OHE), leads to a state of low estrogen symptoms with higher levels of estradiol. 

Sidenote: what do I keep telling myself no matter how bad things can get?  I'm figuring out my body in ways no doctor has yet explained to me (not even Mariano). 

Just got my results in and here's what's up:

Potassium (CMP): 3.9 nmol/L (3.5-5.2)
Potassium (RBC): 79 mEq/L (82-100)
Sodium: 138 nmol/L (136-144)
Chloride: 98 nmol/L (97-106)
Magnesium (RBC): 4.6 mg/dL (4.2-6.8 )
Aldosterone: 1.7 ng/dL (0-30, other studies specify normal range of 4-31 upright)

A few things to note:

- Potassium (serum, non-RBC) has dropped .9 points in the past few years (i.e., before I got sick), and sodium has also dropped a few points as well. 
- Potassium (RBC, i.e., in the blood cells) is technically hypokalemic, but last RBC pull a year ago showed a level of 100; however, according to secondhand study I've found, when the cells uptake potassium like this, this can indicate hypokalmia, but I'm not sure why (if anyone has any insight, that'd be great).
- Sodium is still low (Brownstein recommends 142 as the cutoff for normal), as is chloride, despite drinking .5-1 teaspoons of salt (i.e., sodium chloride) in water daily.
- Magnesium (RBC) is low despite taking 400 mg Mg tablets nightly (i.e., God knows what it would be without this supplement).
- Aldosterone is consistently low, starting with around 7 a year ago, 1.6 after I started hydrocortisone a few months after this, and the number has remained the same (meaning hydrocortisone likely didn't have an effect through downregulation of ACTH, also because aldosterone is only weakly regulated by ACTH).
- Aldosterone was previously taken to reveal below-the-range renin, meaning hyporeninemic hypoaldosteronism (pretty rare), but even weirder this lab pull is I have low potassium where it counts in the cells; potassium is usually inversely related to aldosterone, so wtf?

Any thoughts on why electrolytes would all go down, especially with aldosterone going down as well with potassium?  This nearly one whopping point drop in serum potassium over the years (along with symptoms of fluctuating water retention, possibly fatigue, easy muscle fatigue at times, etc.) has to mean something. 

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