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I’ve been taking 2 drops tyronene and have noticed decreased hunger and feeling cooler in the heat. In a good way. Sex drive is ok but have noticed I’m lasting longer, which is nice.
Interesting... for me, Tyronene isn‘t making me feel cooler but rather making me more comfortable with a higher body temperature.
i read a thread where someone said that a non response to t3 can be a sign of very high nitric oxide levelsYes. But what happens if you use 12,5 mcg every two hours and NOTHING happens? Not even tachicardia? What elements, generally speaking can block the action of T3 at that level?
Very interesting. But what to do against that insensivity? Increase the dose and watch pulse and temperature?i read a thread where someone said that a non response to t3 can be a sign of very high nitric oxide levels
theres a huge list of things that lower nitric oxideVery interesting. But what to do against that insensivity? Increase the dose and watch pulse and temperature?
theres a huge list of things that lower nitric oxide
Aside from methylene blue. What are they?
Just a few options for you;
- caffeine
- Agmatine
- Lysine
- coq10
- Pau D'arco
- Cascara Sagrada/ emodin
- famotidine
- MSM
- b2r5p
- Niacinamide
- adamantane (diamant)
- hydroxy b12
- baking soda
- k1 and k2 quinones
- zinc
Generally speaking too much polyunsaturated fats, high cortisol/estrogen, fluoride, protein deficiency, and endotoxin are the main offenders. There can also be certain nutrient deficiencies, such as magnesium and selenium. Carbohydrate is needed to make liver glycogen, and liver glycogen is needed to convert inactive hormone (T4) into active hormone (T3).
Have you tried taking magnesium with thyroid? Magnesium can help people acclimate to thyroid better than just taking thyroid by itself.I would definitely agree here.
Appetite massively increased, sex drive baseline MUCH higher.
I do notice that having very strong T3 levels, I feel like I pump out a lot of dopamine, Norepinephrine and adrenaline. So there's a little bit of anxiety that accompanies my strong baseline energy.
Yeah those are legitimate concerns, especially the first one in the context of taking oral NDT. Natural desiccated thyroid is bound to a protein, and needs to be digested to become active. Yeah a healthy person, normally on average only produces around 4mcgs of T3 every hour. So an unphysiological dose could cause your liver to deactivate the T3, and in the wrong circumstances, like high cortisol, low glycogen, etc. T4 can also be converted into rT3 instead of T3. I'm not aware of any connection to the body ph, but there could be one. It's not something I've heard Peat talk about extensively. Yeah that's certainly true, as many of the tests like TSH and even T4/T3 don't really examine it's actvivy in the cells. Therefore the blood readings can be less reliable if you also aren't checking things like temp, pulse, feeling of well being, etc. I personally notice thyroid makes me breathe much deeper and easier, when I'm low CO2 (likely from low thyroid) I start hyperventilating.In addition to these possible factors, I wonder whether there are some other possibilities? Eg:
- The particular formulation is not being absorbed into the system, but either just excreted straight out, or damaged in some way during digestion, or is not potent to begin with.
- It's being absorbed, but the body perceives it cannot afford a higher metabolism, so it is blocking the T3 with increased rT3, or some other mechanism I don't know about. Is this something you've looked into?
- Something else is blocking effective metabolism - some internal biochemical process is off it's usual path and is interfering with some area of homeostasis needed for higher metabolism.
- Body pH is too far off.
- The method of measuring metabolic effects is not accurate enough to detect them.
Not being an expert of an, these are just speculations.
if you take too much t3 only, what does it get deactivated into?So an unphysiological dose could cause your liver to deactivate the T3, and in the wrong circumstances, like high cortisol, low glycogen, etc. T4 can also be converted into rT3 instead of T3.
An enzyme is excreted by the liver to deactivate the T3, Peat briefly mentions this somewhere in his email exchanges. I think it just reduces the amount of endogenous T3 being produced, but don't hold me on that, because it's been awhile since I read that email response.if you take too much t3 only, what does it get deactivated into?
in the interview with Georgy and Danny Roddy, Georgy said T3 gets turned into T1 and T2 if it's in excess...
3,5-Diiodo-L-Thyronine (T2) in Dietary Supplements: What Are the Physiological Effects?
Although the ability of T2 to increase metabolism is not in doubt, it is not evident from the published studies what conditions allow for its safe and effective use in humans. This is due in part to the lack of comprehensive human studies, but it is also the result of the fragmented information available in the literature. Published studies often focus on different biochemical or physiological endpoints while using different experimental designs, models, and T2 doses. There is also a considerable bias in the literature towards the beneficial effects of T2, leaving its potential deleterious consequences insufficiently explored. If we consider that its thyromimetic effects may extend to many organs, there is a significant possibility that T2 administration may result in long-term undesirable effects.
In one of the most complete studies available, published in the current issue of Endocrinology (11), Wenke Jonas and investigators in the laboratories of Joseph Kohrle and Annette Schurmann used a mouse model of obesity to analyze the physiological effects of T2. In their thoughtfully designed, carefully performed, and thoroughly discussed experiment, the authors treated obese mice for 2 and 4 weeks with 2 different daily doses of T2 or with a supraphysiological dose of T3 and measured a number of metabolic and physiological endpoints during and after the treatment.
The higher dose of T2 used was 80 times that of T3. Thus, it allows for its estimated lower affinity for the TH receptors, assuming that the affinity of T3 for the receptors is indeed 100 times that of T2 (8). This high dose of T2 essentially mimicked all the physiological effects obtained with the T3 dose. These effects included suppression of the HPT axis, decreases in fat mass, serum leptin and cholesterol, and increases in lean mass, food intake, and hepatic expression of TH-dependent genes relevant to lipid metabolism (see summary of results in Table 1). After 4 weeks, this high dose of T2 also caused cardiac hypertrophy and resulted in elevated metabolic rate and body temperature. These results demonstrate that at a dose that corrects for its decreased affinity for the TH receptor, T2 is capable of producing the same biological effects as T3.
Interesting, Peat explained it much differently. However he didn't really cite anything to back it up, though being just an email it probably didn't occur to him to do so.in the interview with Georgy and Danny Roddy, Georgy said T3 gets turned into T1 and T2 if it's in excess...
+1Have you tried taking magnesium with thyroid? Magnesium can help people acclimate to thyroid better than just taking thyroid by itself.