T2 a Fat Burner for Bulking? 3,5 Diiodo-L-Thyronine Wards Off Fat Gains & Doubles the Number of Hypertrophy-Prone Glycolytic Fast Twitch Muscle Fibers.

Image 1: T2-based fat burners work!
At least when interperitoneally
injected in overfed rats ;-)

Those of you, who followed my writings even in the pre-SuppVersity days may remember my Team-Andro review (original article in German, link is just a google translation) of the purported fat-loss effects of diiodo-L-tyronines. Almost two years ago, I concluded that scientific evidence for their use as "fat burners" in humans was non-existent, while the rodent data that was available at that point, only confirmed that high-dose supplemental 3,5 diiodo-thyronine (and to a lesser extent 3,3' diiodo-thyronine) was able to ameliorate the detrimental metabolic effects of hypothyrodism in rats. Now, the same group of Italian researchers who conducted the initial studies on the metabolic effects of these previously overlooked "by-products" (evidence suggest that they are in fact more than that) of thyroid hormone metabolism, came out with more recent - and certainly way more exciting results (Moreno. 2011).

To assess the effects of 3,5 diiodo-L-thyronine on non-hypothyroid, yet overfed animals, Maria Moreno and her colleagues fed three groups à 15 male Wistar rats (aged 8 weeks, body weight 300+/-5g) either a normal (measured by rat standards ;-) low fat or the infamous high-fat diet, scientists use to induce a pathology that is generally accepted as a model for human obesity and the metabolic syndrome.

Figure 1: Energy content and composition of control and high fat diet in kcal/g of body weight
(data adapted from Moreno. 2011)

Out of the two groups that were fed the hypercaloric high fat diet (cf. figure 1 for a comparison of macronutrient composition and energy content of the diets), one group was injected with 3,5 diiodoL-thyronine at a dose of 25µg/kg (human equivalent: 4µg/kg) interperitoneally. A procedure which turned did not only to reduce or even reverse the detrimental effects of high fat overfeeding on body weight, blood lipids and triglycerides of the animals, but also had direct effects on their muscle fiber composition and muscular glucose uptake via an increased expression of GLUT.4 transporters:

The HFD-induced increases in muscle levels of fatty acid translocase (3-fold; P<0.05) and TGs (2-fold, P<0.05) were prevented by T2 (each; P<0.05 vs. HFD). T2 increased insulin-stimulated Akt phosphorylation levels (~2.5-fold; P<0.05 vs.HFD). T2 induced these effects while sparing muscle mass and without cardiac hypertrophy [both side-effects commonly observed if the same effects are triggered by administration of T3]. T2 increased the muscle contents of fast/glycolytic fibers (2-fold; P<0.05 vs. HFD) and sarcolemmal glucose transporter 4 (3-fold; P<0.05 vs. HFD).

Unfortunately, from a dieters perspective, who will obviously be in a caloric deficit and does not want to ward fat gains off, but to get rid of his/her love-handles, these results are hardly significant. As it was the case in the previous studies by the same group, the model, the scientists used (hyperthyroid animals in previous studies; overfed animals in the study at hand) does not allow for a definitive conclusion on whether or not 3,5 diiodo-L-thyronine, let alone its short acting (cf. Lanni. 1994) "brother" 3,5,3' diiodo-L-thyronine, would facilitate fat loss in healthy (i.e. non-hypothyroid) human beings on a calorically restricted weight loss diet. That being said, the present data allows for the hypothesis that it could ameliorate the detrimental effects of caloric restriction on thyroidal determined parameters of basal metabolism and, at the same time, prevent muscle breakdown via the insulin-dependent upregulation of muscle protein synthesis by increased Akt phosphorylation.

Figure 2: Cholesterol, triglycerides and body weight after 8 weeks of high fat feeding in rats with and without T2 injections relative to values of normal-fed controls (data calculated based on Moreno. 2011)

On the other hand, the study clearly supports the notion that adding T2 to a bulk, i.e. a diet-phase which is intended to increase body, in most cases, muscle mass, could out turn out to be a good idea. The diet used in the study may be called "high fat diet", at the heart, it is however an overfeeding diet; and despite the different macronutrion composition this is not completely different from what body builders will do on a bulk. With appropriate doses (>320µg/day for a 80kg human being) and absorbtion (there is a major difference between interperitoneal injection and oral administration, taken with food, for example T2 could befall a similar fate as levothyroxin (T4) medications, which are to be taken hours away from your last meal to be absorbed properly) T2 could thus ...

• keep you lean due to its beneficial effects on energy expenditure in a state of nutrient overabundance
• help you build & restructure lean muscle via its effects on protein synthesis and muscle fiber type composition [note: a switch towards fast-twitch type-II muscle fibers will not only make you stronger, it will also help you

And since there were no changes observed in the serum levels of the main thyroid hormones T4 and T3, chances are, you could potentially get both these benefits without messing up with your natural thyroid production and without the risk of heart damage or muscle loss, which is a common side effect of using either T3 (both heart damage & muscle loss) or clenbuterol ("just" heart damage) for the exact same purposes, which is decreasing fat gain and increasing type-II to type-I muscle fiber ratio.