Beachbum1546 said:
I'm a type 1 diabetic and I just started clen and T3. I ate a small bowl of oatmeal for breakfast and took my standard dosage of insulin, like I've done for the past 5-6 years. Usually, I have no problems and my blood sugar level is perfect but I checked my blood sugar earlier and it was very high, almost like my insulin didn't work. So, I injected some more insulin, about half the dosage I already took, and an hour has passed by and my sugar level is still high! It was the same sugar level as the first time I checked.
Wtf, I want to lose bodyfat but not at the risk of high blood sugar. If it does decrease insulin sensitivity, should I just stop eating carbs so I don't need to inject insulin at all?
found an intersting article for you--i thought the connection ws strong, but not this critical to each other (thyroid/insulin). they conclude supp insulin w/t-3 in countrproductive, but i am not sure how that would translate to
required insulin supp.....i am going to do some reading..
that said, because of the risk, i think i would ask your doc---
Author Info:
Karl Hoffmann, MS, is a science writer and regular contributor at Cutting Edge Muscle.
Decreased Insulin Secretion
Insulin is well known as a lipogenic hormone. It promotes fat storage by facilitating the uptake of fatty acids by adipocytes, and reducing lipid oxidation in muscle tissue. Several studies have shown that thyroid hormone is associated with glucose intolerance resulting from decreased glucose stimulated insulin secretion (26).
This defect in insulin secretion is believed to result from an increase in the rate of apoptosis (programmed cell death) of pancreatic beta cells as a direct effect of thyroid hormone excess.(27) This process is reversible, since when thyroid hormone is withdrawn the rate of beta cell replication increases until homeostasis returns. However, there are conflicting studies regarding the effects of T3 on insulin. For example, Dimitriadis et al (28) showed a decrease in glucose stimulated insulin secretion, consistent with (25), but an increase in basal insulin. They also observed increased insulin clearance, with a compensatory increase in basal insulin secretion.
So if in fact the hyperthyroid state is associated with lower insulin levels, this could explain a portion of hyperthyroid stimulated lipolysis. The obvious downside here is that insulin is also an anabolic hormone. Basal insulin concentration is thought to limit the action of the ubiquitin-proteasome degradative pathway of muscle protein breakdown (29). Of course supplementing with insulin during T3 use would be counterproductive. However, as mentioned above, anabolic steroids inhibit ubiquitin-proteasome activity, so their use could counter any loss in muscle anabolism resulting from a drop insulin levels.
25) Am J Physiol 1999 Aug;277(2 Pt 1):E370-9 Related Articles, Links Low-dose T(3) improves the bed rest model of simulated weightlessness in men and women. Lovejoy JC, Smith SR, Zachwieja JJ, Bray GA, Windhauser MM, Wickersham PJ, Veldhuis JD, Tulley R, de la Bretonne JA.
(26) Life Sci 2002 Jul 19;71(9):1059-70 Evidence for a deficient pancreatic beta-cell response in a rat model of hyperthyroidism. Fukuchi M, Shimabukuro M, Shimajiri Y, Oshiro Y, Higa M, Akamine H, Komiya I, Takasu N.
(27) Diabetologia 2002 Jun;45(6):851-5 Thyroxine induces pancreatic beta cell apoptosis in rats.
Jorns A, Tiedge M, Lenzen S.
(28) Am J Physiol 1985 May;248(5 Pt 1):E593-601 Effect of thyroid hormone excess on action, secretion, and metabolism of insulin in humans.= Dimitriadis G, Baker B, Marsh H, Mandarino L, Rizza R, Bergman R, Haymond M, Gerich J
(29) Curr Opin Clin Nutr Metab Care 2000 Jan;3(1):67-71 Effects of insulin on muscle tissue.
Wolfe RR.
(30) J Steroid Biochem Mol Biol 2001 Jan-Mar;76(1-5):31-42 Selective modulation of thyroid hormone receptor action. Baxter JD, Dillmann WH, West BL, Huber R, Furlow JD, Fletterick RJ, Webb P, Apriletti JW, Scanlan TS.
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