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Topics - Kierkegaard

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I had been having high E2 symptoms for the last week or more, and about two weeks ago I started taking cough drops for allergies, which suddenly got bad as they often do this time of year in Texas.

Absolutely nothing has changed other than adding adenosylcobalamin (the mitochondrial form of B12, and interestingly since taking this I've noticed a quick loss of 5-6 pounds) and consuming more cough drops.  Well, I look at the ingredients list and what else do I see than "soy lecithin"? 

This is especially troubling seeing how cough drops are lozenges, and as such they bypass liver processing, meaning any ingredients will be more potent given that they hit the bloodstream more easily.

Just a warning for anyone with a cough and sensitive to estradiol.

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? 

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.


Anyone have any recommendations for alternatives to mg doses of anastrozole/Arimidex?  I've heard some people mention anastrozole lozenges, which allow for much lower amounts.  I'm talking only needing to knock my E2 down by 5-15 mg.

Droppers or anything else like that, etc.?

I've been on 6 mg (half an Iodoral tab) of iodine for over a year now and it's offered me benefits in cognition (less brainfog) that's probably attributable to its influence on thyroid function (thyroid hormone *is* tyrosine and iodine working together).  I wanted to see how I felt coming off of it, and about a day or two after coming off of it I noticed a strange metallic taste in my mouth, which almost tastes like the iodine itself. 

Any thoughts or experience with this?  I also have had a few moments of feeling absolutely awful with dissociative-like brainfog and increased fatigue, which seems to have gotten better since trying 1 drop of 2% Lugol's iodine tonight (about 2.5 mg iodine).  Perhaps the decrease in TSH (iodine is known to increase TSH without any known effects) from stopping iodine resulted in a temporary hypothyroid state as TSH "revved up" back to its normal state?

This article provides a great summary of some of the research out there with regard to GSE as an aromatase inhibitor, and this site from Cohen's selfhacked.com site offers a great summary of the man benefits of this powerful supplement.

What I'm wondering is if anyone here has noticed any drop in their estradiol or a reduction in symptoms related to excess estrogen by taking GSE. 

Hey fellas, long time no see. 

Given that many of our neurotransmitters are made from amino acids (according to Jonathan wright), and pepsin -- which is a function of proper digestion and stomach acid secretion -- breaks down proteins into amino acids and so would be useful for a sort of pretest for people with potentially low stomach acid (which is often the case when you have symptoms of dyspepsia like heartburn, which are often erroneously labeled as high stomach acid symptoms -- again I recommend Dr Wright's book on stomach acid here), has anyone here thought of getting comprehensive amino acid testing done?

I got interested in it after putting together the pieces of possible low histidine (amino acid that creates histamine) issues, but then ran into the possibility that the histidine itself could be a function of low carnosine, another amino acid (I'm finding the book The Healing Hutrients Within on amino acids to be a very helpful if a bit too cursory read), so I started looking into comprehensive (i.e., 20-22 amino acids) testing and was surprised to find it was pretty cheap: only $137 dollars at Life Extension: http://www.lifeextension.com/Vitamins-Supplements/itemLC700068/Amino-Acid-Profile-Blood-Test

From my reading it's looking like amino acids (and the low stomach acid that prevents their creation from protein via pepsin) are way overlooked in conventional medicine.  Not only does histidine create histamine (and many people have had paradoxical positive responses to l-histidine supplementation, a few people saying it works better for their allergies than multiple pharmaceutical and otc antihistamines), but tryptophan also becomes 5-HTP and serotonin (which in turn becomes melatonin), and tyrosine becomes l-dopa, dopamine, norepinephrine, and epinephrine, to mention a few. 

Anyone have any experience with testing or supplementation?

https://youtu.be/D9H9qTdserM?t=43m13s -- until 48:15

Quick overview:

-The autonomic nervous system: parasympathetic and sympathetic, and their importance in relation to orgasm. 

-Psychogenic or physiogenic ED; 60% of men who come to doctors for ED are psychogenic, meaning they aren't physical.

-Penile pressure cuff thingy to help determine nocturnal erections (which happen during REM sleep); using stamps is a much better way of measuring.

The whole presentation is outstanding and relates to the title of his equally outstanding book on stress and its many effects on the body, Why Zebras Don't Get Ulcers.  Also good info directly before the timestamp on testosterone and how you need a "thimbleful" and a "few sperm" for fertility.  I recommend the whole lecture. 

Just wanted to post this based on a response to someone who PM'd me.  He is taking choline and l-dopa and wanted to know if these increased norepinephrine and what supplements increase norepinephrine.

Choline becomes acetylcholine, which is the primary neurotransmitter for the parasympathetic nervous system, which counterbalances the sympathetic, which has norepinephrine as its primary neurotransmitter -- meaning good acetylcholine levels are helpful in reducing stress by balancing the parasympathetic with the sympathetic.  Dopa Bean, OTOH, increases your l-dopa, which is used because it increases dopamine.  However, dopamine becomes norepinephrine (and this becomes epinephrine/adrenaline), so there are some people, especially if they take too much, who convert to too much norepinephrine.  I wouldn't let it worry you, and if you want try going off the Dopa Bean for a week and see how you feel, getting back on it, etc. 

L-tyrosine is another supplement that precedes l-dopa, causing the same potential problem in some people too much NE.  Vitamin B6 increases the conversion of l-dopa to dopamine, which again can cause the same thing downstream.  Vitamin C and copper both increase the conversion of dopamine to norepinephrine. 

Remember that we all need a healthy level of norepinephrine, and people actually can get erections and increases in libido from taking buproprion (Wellbutrin) given that it increases norepinephrine.  Orgasms are triggered by norepinephrine release, and a resultant decrease in dopamine, which is one of the main reasons that makes you relaxed after sex.  Norepinephrine is also very important for energy.  Low levels have also been linked to depersonalization and derealization (which some here might know as a type of "brain fog"), especially in combination with low cortisol and/or poor HPA feedback (i.e., the hypothalamus isn't picking up on the signal of cortisol well).

Just FYI.  Norepinephrine and epinephrine are good and necessary within reasonable limits. 

Okay, I'm getting testing done next week (the most friggin' comprehensive testing ever -- literally 3 pages per Mariano, who is awesome) and Mariano asked me to try dropping my iodine dose from 6 mg to 2.5 mg (one drop if Lugol's) and also try stopping quercetin because I'm getting tryptase and histamine pulled (quercetin is a potent mast cell regulator, so much so that it's prescribed for people with Mast Cell Activation Syndrome).  Also, because for the last lab pull I ended up with significantly lower than usual free thyroid levels while on a full dose of quercetin (4 pills/day of Q, which is known to inhibit thyroid at least slightly), in the last few days since doing these changes (iodine to 2.5 mg and quercetin to 2 pills a day), I've been having much more noticeable anxiety.  Not cognitively; I'm feeling it more in my chest, tenser muscles, a few times of irritable bowel, things like that.  I've also been retaining more water and weighing more as a result.  All these symptoms are clearcut "high estrogen" symptoms for me.

Before making these changes I had increased my testosterone dose from 26 mg E3D to 34 mg E3D because my last lab showed low total testosterone and estradiol.  Before making the drops in iodine and quercetin, and after adding PQQ and alpha lipoic acid (for mitochondrial function per Mariano's rec), I was feeling *much better* than I have been -- and well on my way to feeling the best in maybe a full year.

Worth noting that both iodine and quercetin change estrogen metabolism: iodine through draining away 16-hydroxyestrone in favor of estriol (good), and quercetin does it through more peripheral pathways I don't quite understand, but I think the main metabolite of estradiol reduced is 2-hydroxyestradiol, as can be seen here:

From this study: http://hyper.ahajournals.org/content/42/1/82

Also helpful for understanding iodine metabolism via 16-OHE:

So what can I conclude?  Since I've kept all other variables constant, lowering quercetin and iodine seems clearly to contribute to "high estrogen" symptoms.  Yet another reason to think it's not about "absolute" estradiol numbers, but also and in at least some cases more importantly (17b) estradiol metabolites, i.e., how your body processes estrogen.

Anyone have any luck with these?

Examples: https://www.amazon.com/s/ref=nb_sb_noss_2?url=search-alias%3Daps&field-keywords=nitric+oxide+test

Recommendations appreciated. 

From one of his most recent Reddit posts, and it does indeed seem to be supported by the evidence I can actually understand:

Although Vitamin B12 generally contributes to energy generation, is anti-inflammatory (which further contributes to energy), and is important in memory formation, under some circumstances (particularly in excess) it can cause fatigue and impaired cognition.
One prominent mechanism by which this occurs is that Vitamin B12 can bind strongly to Nitric Oxide. At high levels, Vitamin B12 can cause a Nitric Oxide deficiency.

If binding occurs at lower levels of Vitamin B12 but high Nitric Oxide levels, one can also get a relative Vitamin B12 deficiency despite adequate Vitamin B12 levels since Vitamin B12 bound to Nitric Oxide becomes inactive.

Nitric Oxide has many functions including: 1) helping improve circulation providing oxygen and nutrients to muscles and other tissues in the body 2) having anti-inflammatory effects (though it can be pro-inflammatory under certain circumstances). 3) is a reverse neurotransmitter (traveling from dendrites to axons rather than vice versa) important for memory formation.

So a depletion of Nitric Oxide by EXCESSIVE Vitamin B12 can cause fatigue by reducing oxygenation and nutrient transport to cells of the body. It also can result in higher inflammation which can cause fatigue. The Nitric Oxide depletion plus possible excess Vitamin B12 inactivation plus increased pro-inflammatory signaling can impair mental function.

Lesson: Sometimes an excess of Vitamin B12 can be just as bad as a deficit.

This, with Game of Thrones on HBO, is my early Christmas present.  I had no idea these archives existed, and Dr Jonathan Wright is one of the most knowledgeable doctors in the world.  He's the guy who *created* bioidentical estrogen replacement for women, for example (and being the swell person he is he didn't patent it).


His voice is also awesome, so it's perfect for listening before bed. 

Got my results back and my usual free T3 of 3.5-3.7 is down to 2.8 pg/ml (2.0-4.4).  Free T4 is down from usual 1.6-.7 to 1.38 ng/dL (.82-1.77).

These are numbers that are lower than I've ever tested even off of thyroid meds.  So I looked through my symptom tracker notes, and I've added a few supplements in the last few months, during which I've noticed a 10-15 pound increase in water weight (estradiol came back at 20 pg/ml).  These include 200 mg ubiquinol/coq10, 25 mg P5P/B6, 4700 mg (RDA) of potassium citrate (K levels barely budged, sodium is actually at the high end of 4.3), cordyceps mushrooms 1.5 g, 1600 mg quercetin, and in the last week alpha lipoic acid 250 mg.  ETA: I had only been taking ALA one day before getting labs pulled, so it's doubtful it's to blame. 

Both quercetin and ALA have been documented (though I can't find hard research) to slow down the thyroid.  Turns out in looking through my notes, of all my labs that measured thyroid hormones I was only taking quercetin for one of them, and here only for about a week (levels were normal); all other times I wasn't taking Q.  I've never measured thyroid while taking ALA.

Does anyone know if any of the supplements I've mentioned can slow down thyroid this much?  Any research is welcomed. 

My plan now is to come off potassium for a week or two (no really noticeable improvements from it), taper off quercetin over the next few days, but stay on ALA as this is rec'd by Mariano for mitochondrial function (as is cordyceps). 

Per Mariano's "never would have thought of that" recommendations, he's prescribed cordyceps for ATP and other functions.  Since taking it for about a week, one day with pretty heavy lifting (moving a treadmill) that would have involved a full day of post-exertional malaise (feeling more fatigued/foggy/sleepy) only resulted in a few hours if even that.  This positive muscle impact (whatever it is) is exactly why bodybuilders are into this supplement.

However, my weight and blood pressure have been somewhat high, even though part of this is because of allergies, presumably histamine upping estradiol, but things are definitely worse, albeit with some benefits, such as being much more muscular (probably due to the water retention effects of estrogen); either way, it's looking like cordyceps is to blame:

"Cordyceps Militaris supplementation has been shown to increase estradiol levels in rats after 2 weeks of supplementation. By week 4, estradiol levels were back to baseline levels, highlighting Cordyceps role as a “regulator” again, rather than an outright booster. Fortunately, this doesn’t seem to pose any serious threat to men’s T levels as Cordyceps simultaneously increased T while increasing estradiol." (http://supplementsinreview.com/testosterone/cordyceps-testosterone/#increases-estrogen, with reference)

Anyone have any experience with this? 

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