T3/AAS and Insulin Resistance
- 09-05-2006, 12:22 PM
T3/AAS and Insulin Resistance
Simple question: does the use T3 and anabolic steroids separately or in conjunction cause (increase) insulin resistance?
Many times you see people making statements that AAS increase protein synthesis. I have also see statements that suggest T3 increases protein synthesis as well. For the most part I have been able to find data to back these statements up.
I have read of some using T3 in low doses during AAS lean mass/bulking cycles to increase partioning and protein synthesis. But I am also seeing anecdotal evidence that may suggest that T3 used in periods of surplus calories with low to moderate carbohydrate intake (lean mass/bulking) in conjuction with AAS may actually be causing increased insulin resistance.
I'm researching this to see if I can find some data to substantiate the anecdotal evdience that I have seen. But in the meantime, if anyone can provide some feedback or data to support or invalidate this theory. I'm looking for data more than just anecdotal feedback, but either would be helpful.
- 09-05-2006, 07:46 PM
Always a giver...never a receiver
- 09-05-2006, 09:26 PM
Do any of the agents used as ergogenic aids by athletes and bodybuilders cause insulin resistance? Over the years there have been a number of studies done on how androgens affect glucose sensitivity, some of them conflicting. Virtually all studies show that low testosterone causes insulin resistance. One of the most recent studies done in humans showed that supraphysiological testosterone had no effect on insulin sensitivity but nandrolone actually improved it (29). The doses were 300 mg/week.
In another recent study 600 mg of testosterone enanthate per week had no effect on glucose sensitivity in normal adult men (30). This is the highest dose that I've seen used in any studies. However, when 500 mg of testosterone was administered to obese men, glucose tolerance decreased, while 250 mg increased glucose tolerance (31). Obesity could be having an effect here, as the previously mentioned negative studies were done in non-obese individuals.
Hyperandrogenism is often associated with insulin resistance in women. Whether this is merely an association or an actual causal relationship is debated. In agreement with the latter hypothesis, when normal women were administered methyltestosterone, insulin sensitivity deteriorated (32). This could have widespread implications for women’s health as androgen administration becomes more common in the treatment of menopausal symptoms and sexual dysfunction
In other studies in animals, there appears to be a "window" of testosterone levels around the normal range that optimize insulin sensitivity (33).
So you can see why there is some confusion. We don't know what happens when androgen doses exceed 600 mg/week (It is hardly uncommon for bodybuilders to use doses of anabolic steroids far in excess of 600 mg/wk.), and studies in animals have given results in conflict with those done in men, but in agreement with studies performed in women. And the particular compound used seems to make a difference.
One anabolic agent that unquestionably is capable of causing (temporary) insulin resistance is recombinant human growth hormone, hGH. This side effect of hGH is discussed in detail in the M & M # 14 article on GH use to treat obesity, so I will refer interested readers to that piece for more information.
Hyperthyroidism is associated with elevated plasma glucose, and when rats are given high doses of thyroid hormone both fasting glucose and plasma glucose in response to a glucose load are elevated (34). This hyperglycemia does not appear to be the result of any thyroid hormone induced defect in insulin signaling, but rather decreased insulin secretion in response to glucose. The deceased insulin secretion is most likely a result of thyroid hormone induced apoptosis (programmed cell death) of pancreatic beta cells (35). A second factor contributing to the hyperglycemia seen in hyperthyroidism is increased gluconeogenesis (36). So technically, the elevated plasma glucose seen when supraphysiological doses of T3 or T4 are administered is not due to insulin resistance, but rather to lowered insulin production and increased glucose production from glucogenic substrates.
09-05-2006, 09:28 PM
Well, I believe it to be the case from my own experiences. As this is exactly what happened to me. I was telling you this earlier fiddy.
09-05-2006, 09:31 PM
I know, I believe it too.
09-05-2006, 09:38 PM
But I didn't put 2 and 2 together until you mentioned something so I definately have some reworking for my next bulk.
09-05-2006, 10:50 PM
Effect of Testosterone Replacement on Insulin Sensitivity
The effects of androgens on insulin sensitivity have been studied in animal models and the Results of these concur with those observed in men. Castrated male rats exposed to supraphysiological doses of testosterone have increased insulin resistance but, conversely, physiological testosterone replacement improves insulin sensitivity. This implies that testosterone has a major role as a regulator of insulin sensitivity.
The effects of long-term administration of testosterone enanthate on glucose metabolism in rhesus monkeys were studied by Tyagi et al. Nine adult male rhesus monkeys were given 50 mg of testosterone enanthate bimonthly for 32 months and glycaemic control was compared with placebo-treated animals. Significant changes in the glucose tolerance test were not observed in animals treated with testosterone throughout this period. However, serum insulin levels decreased significantly between 27 and 32 months in the testosterone-treated group and returned to baseline values within 3 months of stopping the treatment.
Centol et al. compared serum androgen levels in streptozotocin-induced diabetic rats with controls. The diabetic state produced a marked reduction in serum androgen levels between 10 and 15 days after streptozotocin administration. Further studies with streptozotocin-induced diabetic rats have also shown a similar decrease in testosterone levels, which have been shown to occur as a combination of impaired gonadotrophin secretion at the pituitary level and reduced function of the LH receptor in the testes. Moreover, insulin administration in these diabetic rats partially restored the circulating androgen levels by stimulating testicular 3-beta-hydroxysteroid dehydrogenase activity, thereby enhancing testosterone synthesis as well as receptor binding capacity.
Effect of Anabolic Steroids
Early literature revealed that anabolic steroids lowered fasting blood sugar and reduced glycosuria. The cause for this effect was unknown, although methandienone was reported to enhance insulin secretion. Subsequent research, however, has shown that anabolic steroids adversely affect glucose metabolism. Godsland et al. found that when anabolic steroid methandrostenolone was given to underweight men, insulin action was impaired. Similar Results were also seen when oxymethalone led to impaired glucose intolerance and hyperinsulinaemia in children with idiopathic acquired aplastic anaemia or Fanconi's anaemia. Cohen and Hickman found that powerlifters who ingested anabolic steroids had insulin resistance compared to the nonsteroid-using powerlifters, obese men or nonobese sedentary men. Further evidence of impaired insulin action with high-dose testosterone comes from a study of a transsexual population that included women who chose to become men. The women were treated with high doses of testosterone that resulted in impaired glucose uptake. Thus it would seem that excess androgen and anabolic steroid use reduces insulin sensitivity and impairs glucose tolerance. However, a study in healthy men has shown that nandrolone improved glucose metabolism by enhancing noninsulin-mediated glucose disposal.
Effect of Testosterone Replacement in Hypogonadal Men
No adverse effects of testosterone therapy on insulin secretion or glucose tolerance have been demonstrated in normal men with pharmacologically-induced hypogonadism. Sixty-one eugonadal men between 18 and 35 years of age were randomly assigned to receive monthly injections of long-acting GnRH agonist, to suppress endogenous testosterone secretion, and then given weekly doses of 25, 50, 125, 300 or 600 mg of testosterone enanthate for 20 weeks. In this study no significant effect of testosterone on insulin sensitivity was observed, even though the higher doses of testosterone produced an increase in fat free mass and muscle size. Friedl et al. also demonstrated that pharmacological doses of testosterone and 19-nortestosterone given for 6 weeks to normal men did not impair glucose tolerance.
Testosterone replacement therapy in adult men with hypogonadism improves insulin sensitivity. Simon et al. randomized 18 men to one of three treatment groups – testosterone, dihydrotestosterone and placebo, administered in the form of gel. At the end of 3 months, men receiving androgens had a significantly lower fasting plasma insulin, fasting plasma insulin/fasting plasma glucose ratio, HOMA index and leptin levels. However, in another study of 10 men with idiopathic hypogonadotrophic hypogonadism treated with testosterone, no decrease in insulin sensitivity was observed using the hyperglycaemic euglycaemic clamp method.
A beneficial effect of testosterone treatment on insulin resistance has also been seen in a study in HIV-infected men. Reduced circulating testosterone levels are commonly found in patients with HIV infection and these levels correlate with weight loss and generalized muscle wasting. Sattler et al. compared the effects of nandrolone decanoate and resistance training in 30 HIV-infected men over a 3-month period. Those patients who received both treatments had significantly lower fasting insulin and glucose levels and HOMA index. However, these changes were transient, with the metabolic effects returning to baseline 2 months after treatment was withdrawn.
Effect of Testosterone Treatment in Obese Men
Intra-abdominal fat may be a part of the pathway through which lower testosterone level is related to insulin resistance. Marin et al. examined the effects of testosterone administration in middle-aged obese men. Reduced glucose tolerance was observed 1 week following intramuscular injection of 500 mg testosterone (producing supraphysiological plasma levels of testosterone). However, following treatment with doses achieving plasma levels high in the physiological range, plasma levels of insulin were reduced and insulin sensitivity increased. The greatest effect was observed in menwith lower baseline testosterone levels. In another study by the same group, 23 middle-aged abdominally obese men were randomized to 8 months of treatment with testosterone and placebo. Testosterone treatment led to reduced insulin resistance. These changes could be due either to the effects of testosterone on visceral fat or to a direct effect on muscle insulin sensitivity.
Effect of Testosterone Replacement in Diabetic Men
Men with type 2 diabetes have a higher prevalence of hypogonadism, as mentioned earlier. Testosterone is an important modulator of insulin sensitivity and the consequences of improved insulin sensitivity in diabetic subjects is better glycaemic control. There are, however, few interventional studies that have been performed in this group of patients. Boyanov et al. assessed the effects of oral testosterone supplementation in 48 type 2 diabetic men with mild androgen deficiency. Twenty-four men received testosterone and the other 24 men were given placebo. Oral treatment with testosterone resulted in a significant reduction in body weight, body fat, blood glucose and mean glycated haemoglobin (from 10·4% to 8·6%). Even though this was a nonblinded study and oral testosterone was used, favourable effects of testosterone treatment on the metabolic parameters in type 2 diabetic men were observed. However, although Corrales et al. also found a high prevalence of hypogonadism in type 2 diabetic men, a neutral effect on glycaemic control with intramuscular testosterone replacement therapy was observed in 10 type 2 diabetic men with partial androgen deficiency.
09-06-2006, 12:23 AM
And before I go to bed I leave you with this...
Grow it long, shave it Bare
Life is hard, never Nair
I need a razor, I need it quick
Before this cream makes me sickStrap it on, Tear it off
She wants it hard, not you soft
I need a break, I need it quick
Before this freak makes me her *****
09-06-2006, 09:35 AM
09-06-2006, 12:20 PM
Let me work my mojo!
09-06-2006, 01:02 PM
Where the hell is Bobo at? He's good at this stuff and much smarter than Admin who couldn't answer something this technical.
09-06-2006, 01:04 PM
HRT and insulin sensitivity - Cutting Edge Muscle Forums
Originally posted by Nandi
I think in general androgens and estrogens both reduce body fat, although there are conflicting studies in both cases. Fat depot location has to be considered as well. Most studies show androgens decreasing subcutaneous fat, while some studies show testosterone decreases visceral fat, and others show an increase in visceral fat.
As far as insulin sensitivity and androgens goes, the data are too inconsistent to draw any conclusions, IMO, except in the the case of hypogonadism where HRT does seem to improve insulin sensitivity. We discussed some studies dealing with androgens and insulin sensitivity in a recent thread:
Cutting Edge Muscle Forums
This is a decent review of the existing data on sex steroids and insulin resistance:
Clinical Science (2002) 102, 151-166 - C. Livingstone and M. Collison - Sex steroids and insulin resistance
09-06-2006, 01:08 PM
heh...I see our short chat sparked some great interest. I'll be reading.
09-06-2006, 01:08 PM
I'm going to my "real" job for sevaral hours to milk the clock for some overtime. When I get back I expect answers!!!
09-06-2006, 06:45 PM
09-06-2006, 07:06 PM
T4/T3 Sticky anabolic review
There's a sticky in anabolic reviews gh/slin/ that has some info on that.Originally Posted by B5150
09-06-2006, 07:10 PM
HGH is used long term, does that still mean insulin sensitivity is temporarily decreased?Originally Posted by B5150
09-06-2006, 07:27 PM
Is that link working? I can't access their site today.
EDIT: Nevermind. I chnaged my security and it allowed me on. I'm not happy that some of the sites that I used to frequent have changed so that I have to reduce my security controls to access them.
09-06-2006, 07:30 PM
Quite a load to digest.
I am on HRT. I take HGH 2iu 2X/day. I take 25mg DHEA 2x/day. I have added cinnamin, ALA and chromium to increase insulin sensitivity because of my age. I took a glucose tolerance test and was high normal. at 58 yrs old. In addition I have started doing 5iu insulin PWO. I have been looking for the very info you have provided. I am considring stopping PWO insulin and doing 2iu before each of my three main meals. The beta cell burn out is my main concern. Thanks for the very indepth research material. B5150Originally Posted by B5150
PS I take 50mcg T4 daily to boost HGH performance.
09-06-2006, 07:36 PM
Mine just did this too B, what the hell caused this?
09-06-2006, 07:40 PM
I hate to jump to conclusions, but my first thoughts are ad-aware and spy-ware type of things. They have a whole lot of advertisers on that board as well. I try to dump my cache as often as I can remember.
09-06-2006, 07:42 PM
Feel free to clean this up B so it can get back to the topic. I would like to see more input from people.
09-06-2006, 07:42 PM
I lied...I love to jump to conclusions
09-06-2006, 07:44 PM
Wait a second?! You mean I actually have administrative controls?Originally Posted by Jayhawkk
09-06-2006, 07:48 PM
No, you have temporary editing abilities granted by me with a time limit!
09-07-2006, 12:09 PM
Thyroid hormone stimulated glucose uptake in human mononuclear blood cells from normal persons and from patients with non-insulin-dependent diabetes mellitus.
Kvetny J, Matzen L.
Department of Clinical Chemistry and Internal Medicine S, Odense University Hospital, Denmark.
Thyroxine and T3 induced oxygen consumption and glucose uptake were studied in vitro in mononuclear blood cells isolated from patients with non-insulin-dependent diabetes mellitus (NIDDM) and from non-diabetic control persons. Cellular oxygen consumption and glucose uptake were promptly increased by physiological and supraphysiological concentrations of T3 and T4 in a dose-dependent manner (50-5000 nmol/l), whereas rT3 and T2 had no stimulatory effect. The effect of T3 and T4 was independent of new protein synthesis in that it was not blocked by tunicamycin (1 mg/l) and tiothepa (75 mg/l). Examination of stimulation of cells from control subjects and patients with NIDDM revealed an identical oxygen consumption, whereas the thyroid hormone-induced glucose uptake was significantly increased in cells from patients with NIDDM. T4 (5 mumol/l) stimulation in controls: 1.34 +/- 0.23 mmol.l-1 (mg DNA)-1.h-1, in NIDDM: 3.24 +/- 0.77 mmol.l-1.(mg DNA)-1.h-1, P less than 0.05 (mean +/- SD). These studies indicate that T4 as well as T3 increases cellular oxygen consumption and glucose uptake and that this stimulation is independent of new protein synthesis. Examination of cells from patients with NIDDM revealed an increased thyroid hormone induced glucose uptake, indicating increased thyroid hormone sensitivity. This observation contrasts the well known insulin insensitivity, suggesting separate mechanisms for glucose uptake elicited by insulin and thyroid hormones.
PMID: 2499151 [PubMed - indexed for MEDLINE]
09-11-2006, 07:48 PM
Well, I was at thebetterbodybuildingboard.com and they said that you guys were all poopie heads.
10-04-2006, 01:00 AM
Would that mean that one's glucose levels would be higher than normal or that one's pancreas would simply be forced to produce more insulin?
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