How to fix a slow metabolic rate: excessive hunger, and low energy

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Hans

Hans

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I don't know if others had the same experience than me, or if there are confounding factors at play, but colloidal gold rather seems to induce hyperphagia than reducing hunger, for me.
Interesting. Perhaps it's very pro-metabolic for you. It's highly conductive.
 

Osukhan

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have been taking Tudca for about a month, and i believe i have Ormus Gold and will add it to the mix
 

LLight

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@Hans maybe.
Or other factors are at play and my conclusions are wrong. Maybe hyperphagia is not the proper term, but I'm more hungry than usual.

Thanks.

Ps: I believe I was also more intellectually active today than normally, so the metabolic improvement may be true.
 

LLight

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I'm not sure how to interprete this study. It mentions that gold could impair the job of the DIO1 enzyme but relatively to reverse T3. Could it be not the case for normal T3? Maybe there is nothing to be understood from the abstract alone.

How do you understand it @Hans? Thanks
 

LLight

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Maybe DIO1 (relatively to other DIO enzymes) is not that important and could lead to rT3 more than T3. Its precise role may be not totally known as I've just read.
 

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The functional role of D1 in humans remains a matter of debate. Nearly 80% of peripheral T3 originates from deiodination of the pro-hormone T4 by D1 and D2. However, the relative roles of D1 versus D2 in extrathyroidal T3 production are still controversial. Probably because D1 was the first selenodeiodinase to be identified and because of its subcellular location, it was often assumed that the majority of circulating T3 was derived from T4 via D1 activity. Nevertheless, the long-life of D1 protein and T3 upregulation of D1 activity, just the opposite of what would be expected in a typical feedback loop, raise some questions about this assumption. Moreover, clinical studies have showed a maximum decrease of 25% in serum T3 in athyreotic, T4-replaced, euthyroid individuals treated with higher doses of PTU (Geffner et al. 1975, Saberi et al. 1975). Indeed, subsequent cumulative data on the biochemical and molecular properties of D2 indicate that this enzyme also contributes a significant portion of serum T3 levels in humans (Bianco et al. 2005, Maia et al. 2005). The D1 enzyme seems extremely inefficient in carrying out this reaction when compared with the D2, which has a 700-fold greater catalytic efficiency for 5′-deiodination of T4 (Maia et al. 2005). First, in contrast with D2-catalyzed reaction that generates 1 mol of T3 for each T4 molecule, for each 2 moles of T4 deiodinated by D1, only 1 mol of T3 and a second of rT3 is produced since D1 catalyzes the inner- and outer-ring deiodination of T4 equally well, as predicted from Vmax/Km estimates (Visser et al. 1988). This can explain a catalytic efficiency difference of 2, whereas the rest is primarily due to the much slower rate of D1-catalyzed T4 to T3 conversion under physiological conditions. This is not easily observed under typical in vitro assay conditions because the catalytic activity of this enzyme significantly varies from the artificial DTT generally used to other cofactor candidates such as GSH, as well as with variations of the cofactor concentrations (Goswami & Rosenberg 1987, Goemann et al. 2010).
 
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Hans

Hans

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I'm not sure how to interprete this study. It mentions that gold could impair the job of the DIO1 enzyme but relatively to reverse T3. Could it be not the case for normal T3? Maybe there is nothing to be understood from the abstract alone.

How do you understand it @Hans? Thanks
Yes I was going to say the same as what you found. DIO1 creates both T3 and rT3, and gold seems to reduce the conversion to rT3.
 
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