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Testosterone Replacement, Low T, HCG, & Beyond
Blood Test Discussion
High estrogens / SHBG
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<blockquote data-quote="Castaneda" data-source="post: 147822" data-attributes="member: 36807"><p>No time for a prolonged update now, but the problem was SR Liothyronine, as I had suspected. I skipped the second dose right after the last post and went straight for 5mcg of the Liothyronine drops I had been using before. Within just 15 minutes, all symptoms disappeared and I was back to baseline. Within 30 minutes, temps were at 98.2 again. Next morning, I was completely back to normal.</p><p></p><p></p><p></p><p>I will say this --- between 5mcg, 10mcg, and 15mcg Liothyronine SR from Empower, none of them produced any noticeable result. If I take, for example, just 1-2 drops of my Liothyronine solution sublingually, it is tangible. Heart-rate goes up slightly and temps respond. Nonetheless, 5mcg is the minimum dose for me to feel "normal". So if, for example, the 15mcg T3 SR were bound to a medium that was releasing liothyronine over, say, a 12 hour period, then we would see only ~1-2mg per hour over that period. To get 5mcg levels sustained, I'd have to take 5x that dose in SR format. That would be 75mcg SR, and the highest dose most pharmacies consider for SR is 35mcg. Then there is the question of the potential for severe spikes as a result of inconsistent release. At that level, it would be risky business. Hell, it's risky business taking more than 5mcg instant release at a time, IMHO. Double that risk for sublingual route.</p><p></p><p>I have samples of all three of the Empower SR capsules (5,10,15) and will be sending them off for analysis later this week (simply to satisfy my curiosity about them). As for a compounding pharmacy "knowing how to make SR T3", there is no way to know without testing their output. In my own experience (with the labs where we run experiments), the only consistent results were seen with liposomes and drug-polymer conjugates (e.g. hydrogels). The powdered excipients, as [USER=23875]@Mark Saur[/USER] mentioned, are not consistent. This is a question of how they are being broken down along the digestive tract. My GI system is relatively clean, according to recent testing, but there could conceivably be some fermentation of foods or other issues that prevent proper degradation. That would be the only explanation -- apart from a lack of medication bound to the excipient.</p><p></p><p>I have no desire at this point to go after prescription Cytomel, brand name or generic. The drops I am using are working perfectly fine. The big challenge for me now is titrating up to the desired 50mcg total / day, since over 5mcg instant release I get palpitations. I have considered mixing it with short-chain fatty acids and ethanol and using topically. I have done that with other substances in the past and get fairly good results. </p><p></p><p>Also, I failed to mention that I also ordered Cialis SR through Empower and got no result from that as well, so chances are high that I'm not breaking down the SR excipient properly. I can't imagine other people aren't encountering similar issues.</p><p></p><p></p><p></p><p>Apologies this was not clear. This is the line-up right at this moment:</p><ul> <li data-xf-list-type="ul">Testosterone Cypionate liposomal cream transcrotally (100mg BID)</li> <li data-xf-list-type="ul">Liothyronine USP, 5mcg, 5x / day sublingually</li> <li data-xf-list-type="ul">Progesterone / DHEA in tocopherols, 5mg/5mg, QD before bed</li> </ul><p>Nothing else.</p><p></p><p></p><p></p><p>Odd, how did you come to the conclusion I am measuring progress in minutes or hours? My methodology looks at subjective results once weekly with labs monthly or bimonthly. That's it. My updates here on the forum are few and far between. I am a mental health professional (with a focus in neurobiology). The majority of people in that particular field have their head stuffed halfway up their rear ends, prescribing Xanax and SSRIs to unsuspecting people with anxiety / depression. If you want to talk about the biology of anhedonia, please, that's in my wheelhouse. I'm all ears. I presume you will also tell my patients with Parkinson's and Alzheimer's that their neurodegeneration is also in their heads, yes?</p><p></p><p>Neuroendocrine dysregulation is neither exclusively in the head nor between the legs. It's both. Treating one or the other in isolation only leads to trouble. Sometimes, we don't lay all of our cards on the table, so as not to confuse matters. There are holes in my knowledge of endocrinology. I am here to connect dots. </p><p></p><p></p><p></p><p>Yes, what I was referring to is the lack of T3 present to counteract already high RT3. I don't want to drag this thread into the deep research I've been doing with immunological pathways and autoimmunity. I'm quite sure I understand what's pushing my naturally normal-high T4 to RT3, but that's a separate affair. My RT3 was going up on SR T3 because of the absence of <em>a sufficient concentration of T3</em> over time. That being said, 30mcg of my solution spread over ~16 hours, while stabilizing temperatures and getting heart-rate up, still does not bring down RT3 to the single digits, so I have some thinking to do regarding the proper approach. Topical route might be the answer, somewhat more predictable than GI tract. Increasing number of sublingual doses would also work to keep levels consistent, but a logistical nightmare.</p><p></p><p>I'm going to probably need to look into liposomal compounding. If there are enough people struggling with SR, then there may be a justification to secure funding for a more formal offering. As for what to do about my high SHBG, I haven't heard any plausible theories on that one yet. Why is the liver increasing SHBG output? I still say it does that in a Th2-skewed immune profile where histamine, mast cells, and estrogen are conspiring with each other. </p><p></p><p><a href="https://www.frontiersin.org/articles/10.3389/fimmu.2012.00169/full" target="_blank">Role of female sex hormones, estradiol and progesterone, in mast cell behavior</a></p><p></p><p>My pattern --- estradiol rises, mast cell destabilization, <a href="https://www.ncbi.nlm.nih.gov/pubmed/26797518" target="_blank">astroglial / microglial activation</a>, induction of <a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3379540/" target="_blank">Herpes and EBV viral lytic cycle</a>. HSV-2 fever blisters appear in various areas during this cycle combined with hypersensitivity to foods, allergens, etc. How do you capture that on a lab when SHBG is surging up to bind a great deal of it (estrogens)? The lab will show "normal-high" estradiol. Men need to start thinking about these things, especially if they have a history of asthma. None of the hormone docs get it. Do you think this profile could also cause oxidative stress to dopaminergic neurons and lower hedonistic tone / i.e. wreck the "reward pathway"? Yes. And consider this:</p><p></p><p><a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3158742/" target="_blank">Effects of thyroid hormone on HSV-1 gene regulation: implications in the control of viral latency and reactivation</a></p><p></p><p>Consistent immune activation leads to high RT3 which leads to less inhibition of viruses which leads to.... you guessed it. This isn't overthinking. This is the key to understanding the neuroendocrine disruptions in a large number of men that aren't responding to T therapy. Problem is, none of it is clear when your RT3 is high. LOL.</p></blockquote><p></p>
[QUOTE="Castaneda, post: 147822, member: 36807"] No time for a prolonged update now, but the problem was SR Liothyronine, as I had suspected. I skipped the second dose right after the last post and went straight for 5mcg of the Liothyronine drops I had been using before. Within just 15 minutes, all symptoms disappeared and I was back to baseline. Within 30 minutes, temps were at 98.2 again. Next morning, I was completely back to normal. I will say this --- between 5mcg, 10mcg, and 15mcg Liothyronine SR from Empower, none of them produced any noticeable result. If I take, for example, just 1-2 drops of my Liothyronine solution sublingually, it is tangible. Heart-rate goes up slightly and temps respond. Nonetheless, 5mcg is the minimum dose for me to feel "normal". So if, for example, the 15mcg T3 SR were bound to a medium that was releasing liothyronine over, say, a 12 hour period, then we would see only ~1-2mg per hour over that period. To get 5mcg levels sustained, I'd have to take 5x that dose in SR format. That would be 75mcg SR, and the highest dose most pharmacies consider for SR is 35mcg. Then there is the question of the potential for severe spikes as a result of inconsistent release. At that level, it would be risky business. Hell, it's risky business taking more than 5mcg instant release at a time, IMHO. Double that risk for sublingual route. I have samples of all three of the Empower SR capsules (5,10,15) and will be sending them off for analysis later this week (simply to satisfy my curiosity about them). As for a compounding pharmacy "knowing how to make SR T3", there is no way to know without testing their output. In my own experience (with the labs where we run experiments), the only consistent results were seen with liposomes and drug-polymer conjugates (e.g. hydrogels). The powdered excipients, as [USER=23875]@Mark Saur[/USER] mentioned, are not consistent. This is a question of how they are being broken down along the digestive tract. My GI system is relatively clean, according to recent testing, but there could conceivably be some fermentation of foods or other issues that prevent proper degradation. That would be the only explanation -- apart from a lack of medication bound to the excipient. I have no desire at this point to go after prescription Cytomel, brand name or generic. The drops I am using are working perfectly fine. The big challenge for me now is titrating up to the desired 50mcg total / day, since over 5mcg instant release I get palpitations. I have considered mixing it with short-chain fatty acids and ethanol and using topically. I have done that with other substances in the past and get fairly good results. Also, I failed to mention that I also ordered Cialis SR through Empower and got no result from that as well, so chances are high that I'm not breaking down the SR excipient properly. I can't imagine other people aren't encountering similar issues. Apologies this was not clear. This is the line-up right at this moment: [LIST] [*]Testosterone Cypionate liposomal cream transcrotally (100mg BID) [*]Liothyronine USP, 5mcg, 5x / day sublingually [*]Progesterone / DHEA in tocopherols, 5mg/5mg, QD before bed [/LIST] Nothing else. Odd, how did you come to the conclusion I am measuring progress in minutes or hours? My methodology looks at subjective results once weekly with labs monthly or bimonthly. That's it. My updates here on the forum are few and far between. I am a mental health professional (with a focus in neurobiology). The majority of people in that particular field have their head stuffed halfway up their rear ends, prescribing Xanax and SSRIs to unsuspecting people with anxiety / depression. If you want to talk about the biology of anhedonia, please, that's in my wheelhouse. I'm all ears. I presume you will also tell my patients with Parkinson's and Alzheimer's that their neurodegeneration is also in their heads, yes? Neuroendocrine dysregulation is neither exclusively in the head nor between the legs. It's both. Treating one or the other in isolation only leads to trouble. Sometimes, we don't lay all of our cards on the table, so as not to confuse matters. There are holes in my knowledge of endocrinology. I am here to connect dots. Yes, what I was referring to is the lack of T3 present to counteract already high RT3. I don't want to drag this thread into the deep research I've been doing with immunological pathways and autoimmunity. I'm quite sure I understand what's pushing my naturally normal-high T4 to RT3, but that's a separate affair. My RT3 was going up on SR T3 because of the absence of [I]a sufficient concentration of T3[/I] over time. That being said, 30mcg of my solution spread over ~16 hours, while stabilizing temperatures and getting heart-rate up, still does not bring down RT3 to the single digits, so I have some thinking to do regarding the proper approach. Topical route might be the answer, somewhat more predictable than GI tract. Increasing number of sublingual doses would also work to keep levels consistent, but a logistical nightmare. I'm going to probably need to look into liposomal compounding. If there are enough people struggling with SR, then there may be a justification to secure funding for a more formal offering. As for what to do about my high SHBG, I haven't heard any plausible theories on that one yet. Why is the liver increasing SHBG output? I still say it does that in a Th2-skewed immune profile where histamine, mast cells, and estrogen are conspiring with each other. [URL='https://www.frontiersin.org/articles/10.3389/fimmu.2012.00169/full']Role of female sex hormones, estradiol and progesterone, in mast cell behavior[/URL] My pattern --- estradiol rises, mast cell destabilization, [URL='https://www.ncbi.nlm.nih.gov/pubmed/26797518']astroglial / microglial activation[/URL], induction of [URL='https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3379540/']Herpes and EBV viral lytic cycle[/URL]. HSV-2 fever blisters appear in various areas during this cycle combined with hypersensitivity to foods, allergens, etc. How do you capture that on a lab when SHBG is surging up to bind a great deal of it (estrogens)? The lab will show "normal-high" estradiol. Men need to start thinking about these things, especially if they have a history of asthma. None of the hormone docs get it. Do you think this profile could also cause oxidative stress to dopaminergic neurons and lower hedonistic tone / i.e. wreck the "reward pathway"? Yes. And consider this: [URL='https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3158742/']Effects of thyroid hormone on HSV-1 gene regulation: implications in the control of viral latency and reactivation[/URL] Consistent immune activation leads to high RT3 which leads to less inhibition of viruses which leads to.... you guessed it. This isn't overthinking. This is the key to understanding the neuroendocrine disruptions in a large number of men that aren't responding to T therapy. Problem is, none of it is clear when your RT3 is high. LOL. [/QUOTE]
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Testosterone Replacement, Low T, HCG, & Beyond
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High estrogens / SHBG
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