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olddawg
06-11-2013, 05:53 PM
by Karl Hoffman


One of the more commonly encountered assertions in the bodybuilding literature is that anabolic steroids (AAS) suppress thyroid function. What is the origin of this claim? Is it supported by evidence published in the scientific literature? And perhaps most important is it of any clinical significance, meaning if it does occur is it serious enough to worry about? Before reviewing the evidence for and against AAS induced thyroid impairment a short review of thyroid physiology is probably in order.

The thyroid gland secretes principally the hormone thyroxine (T4) along with small amounts of triiodothyronine (T3). The majority of the T3 in the circulation (about 80%) is formed from the conversion of T4 to T3 by the enzyme deiodinase. Most of this transformation takes place in the liver and kidney. T3 is considered the physiologically active hormone; in this sense T4 can be thought of as a prohormone.

The production within and secretion from the thyroid gland of T4 is under the control of Thyroid Stimulating Hormone (TSH), which is secreted from the pituitary gland. Higher levels of TSH lead to higher rates of hormone production and secretion from the thyroid. TSH in turn is regulated by another hormone secreted from the hypothalamus, thyrotropin-releasing hormone (TRH). TSH levels are also regulated in a negative feedback manner by the levels of circulating thyroid hormone. If extra hormone is administered, transcription of the TSH gene is decreased and less TSH is produced by the pituitary, leading to suppression of natural thyroid hormone production. Similarly, a decrease in the rate of thyroid hormone secretion leads to enhanced TSH production in an attempt to return to homeostasis.

Just as the bulk of circulating androgens and estrogens are bound to sex hormone binding globulin (SHBG), most of the thyroid hormone in circulation is bound to thyroid binding globulin (TBG). And as with SHBG and sex hormones, the levels of TBG influence the levels of total thyroid hormone in circulation. If TBG is depressed, total T4 and T3 levels will go down. An increase in TBG leads to higher values of total thyroid hormone. Note however that the small percentage of T3 and T4 that remain unbound to TBG (0.05% of T4 and 0.5% of T3), the so-called free fraction, is the portion considered physiologically active. So it is quite possible to have lowered total T3 if TBG is low, but still have normal levels of free T3. This condition is not indicative of thyroidal impairment since the bioactive free T3 is normal. Similarly when TBG is elevated total T4 and T3 are high, again with the possibility that physiologically active free hormone levels remain normal.

A number of drugs and medical conditions are capable of elevating TBG and hence total T4 and T3 levels. These include estrogen, oral contraceptives (OC), pregnancy, acute infectious hepatitis, and cirrhosis. Likewise there are drugs and medical conditions that lower TBG. These include cortisol, growth hormone, and very important to this discussion, anabolic steroids. So to recap, if a person were using AAS and had their total T4 and T3 measured, because TBG is low, those total values would register as low, but that would not necessarily mean that the bioactive (free) levels of T3 and T4 are low. This observation will be critical to our discussion of the effects of AAS on the thyroid gland. In a similar vein, a woman using OC might have elevated T4 and T3 because oral contraceptives raise TBG. This would not necessarily warrant a diagnosis of hyperthyroidism, as her free thyroid levels could be perfectly normal.

So we see that in order to assess thyroid function, measuring only the total T4 and/or T3 is inadequate because these values are strongly influenced by TBG levels. Other laboratory tests are required to determine whether low T4, say, is being caused by actual hypothyroidism, or reflects the use of a drug that is simply lowering TBG. One such test is the thyroid hormone binding ratio (THBR; T3 resin uptake). This test is essentially a measure of the number of TBG sites that are occupied by thyroid hormone. In a person who is hyperthyroid (high T4) there are fewer unbound TBG sites/more occupied sites (since obviously there is more thyroid hormone available to bind to them). In this case T3 resin uptake is high. Conversely, in hypothyroidism there are fewer occupied TBG binding sites, and T3 resin uptake is low. In the case where thyroid function is normal but TBG is elevated (oral contraceptives) it turns out T3 resin uptake registers LOW; conversely when TBG is lowered (AAS use), a lab report would show T3 resin uptake reading HIGH.

We can tabulate these various possible outcomes to give a clearer picture of how these two tests can be used to distinguish thyroid dysfunction from mere altered levels of TBG:


SERUM T4 SERUM T3 T3 RESIN UPTAKE
Hyperthyroidism High High High
Hypothyroidism Low Low Low
Normal, on OC High High Low
Normal, on AAS Low Low High


TABLE 1

Perhaps the test most commonly performed test to determine thyroid status measures Thyroid Stimulating Hormone (TSH) levels. Typically in hypothyroidism, the thyroid is not secreting adequate levels of T4, and in an attempt to stimulate the thyroid, the pituitary secretes excess TSH. So in hypothyroidism, TSH is HIGH. The opposite is observed in hyperthyroidism: the excess thyroid hormone in circulation acts back on the pituitary to suppress TSH production. TSH is LOW in hyperthyroidism.

The above applies to so-called primary hypothyroidism/hyperthyroidism where the thyroid gland itself is malfunctioning. In secondary hyper/hypothyroidism the problem lies at the levels of the pituitary or hypothalamus. In this case the pituitary secretes insufficient TSH to stimulate the thyroid, resulting in hypothyroidism with low TSH. In secondary hyperthyroidism the pituitary secretes excess TSH, resulting in hyperthyroidism associated with elevated TSH.

Before the advent of highly sensitive TSH assays, it was common to perform a TRH challenge test. Recall the hypothalamus secretes TRH, in turn stimulating the pituitary to secrete TSH. In the TRH test, a bolus injection of synthetic TRH is administered. The body’s normal response is to secrete increased levels of TSH up to a peak at 20 minutes and then to decrease TSH secretion. In hyperthyroidism, TSH is being suppressed by circulating thyroid hormones so there is a suppressed response to TRH. In primary hypothyroidism, which is due to thyroid dysfunction with normal pituitary function, levels of thyroid hormones are very low and TSH levels are ordinarily raised; however, TSH increases greatly on TRH stimulation yielding an exaggerated response - it reaches a higher peak and does not decline for over an hour. In secondary hypothyroidism (where the pituitary is malfunctioning, not the thyroid) it doesn't matter how much TRH there is, the pituitary cannot make TSH so there is an absent response to TRH stimulation.

Now that we have reviewed the elements of thyroid physiology and gone over the basic tests to determine thyroid function, we are ready to review the literature regarding the effects of anabolic steroids on the thyroid. At the beginning of this review, we asked the question “what is the origin of the claim that AAS impair the thyroid?� The answer perhaps lies in a 1993 paper by Deyssig & Weissel (1). The authors looked at the effects of self-administered AAS use in an admittedly small group of five bodybuilders. Eight additional subjects served as controls. In the AAS using group, total T4, Total T3, and TBG were depressed relative to the control group. Recall this is consistent with the widespread observation that by lowering TBG, AAS lower total T4 and total T3 with no effect on the free hormone levels and hence no effect on TSH. Indeed in this study there was no difference in free T4 and TSH between the AAS group and the controls. Basal free T3 was not measured. So far everything is consistent with normal thyroid function accompanied by AAS induced depression of TBG.

The authors next performed a TRH test. Upon administration of THR, TSH values climbed significantly higher in the AAS group, and the T3 response was significantly lower in the AAS group. Recall that in hypothyroidism there is an exaggerated TSH response to TRH. Quoting from the study, “These T3 and TSH reactions to TRH point to a mild impairment of thyroid function as a consequence of the use of anabolic steroids.� However, stressing the fact that all unstimulated parameters were consistent with the simple suppression of TBG by AAS, the authors conclude that “the results of our cross-sectional study show that high doses of androgenic-anabolic steroids, as are used by some athletes, may impair thyroid function to an extent that is not clinically detectable and probably not relevant.� (Italics added.)

Moreover, when one scrutinizes the data, one sees that out of the five AAS-using subjects, only two had stimulated TSH values higher than the controls, one was only marginally but not significantly higher than in controls, and two had stimulated TSH values in the control range. In addition, no pre-study baseline stimulated TSH values were measured in any subjects. One could argue these facts call into question the authors’ conclusions of “mild impairment of thyroid function�.

How high were the “high doses� used by the participants? The subjects were using a number of different AAS including testosterone, nandrolone, stanozolol, and Dianabol, stacking them as bodybuilders typically do. The average total dose for all drugs combined was 1.26 grams/week, with a range of 740 – 1950 mg/week.

Alen et. al. (2) conducted a study along similar lines. Seven power athletes stacking testosterone, Dianabol, stanozolol, and nandrolone were monitored for (among other things) thyroid function during a 12 week period. In this study, total T3, total T4 and TBG were all depressed during the study period, while T3 resin uptake was elevated. All of these changes are again consistent with AAS induced suppression of TBG, with no direct effect on thyroid function. Interestingly, TSH dropped during the first 8 weeks of the study, and then began to climb. Free T4 dropped marginally but stayed within the normal range. The authors interpreted the data thusly:


It is tempting to suggest that decreases in serum TBG led to decreased protein binding of the thyroid hormones, T4 and T3, which is reflected in the elevated T3U-values [T3 resin uptake]. Increased availability of T4 and T3 would then lead to a compensatory decrease in serum TSH, and this, via decreased thyroid stimulation, would further decrease total concentrations of circulating T4 and T3. The measurements of thyroid function parameters performed support this reasoning. In general our findings suggest that thyroid hormones at the cellular level were not disturbed in our athletes.

While the approximate 20% drop in free T4 observed by Alen et al is suggestive of some degree of thyroid impairment, the consequences of this need to be interpreted carefully. First, free T4 stayed well within the normal range. Second, since free T3 was not measured, we do not know if there was any change in free T3, the metabolically active hormone. Lum et al. have shown that when serum T4 levels drop, the body upregulates the peripheral conversion of T4 to T3, maintaining metabolic homeostasis (3). So it is possible that any drop in free T3 could have been significantly smaller than the observed 20% drop in free T4.

We see here contradictory findings between the two studies discussed so far as regards TSH levels: Deyssig & Weissel observed no change in unstimulated TSH levels, while Alen et al observed a decline in TSH, although the values remained well inside the normal range. The finding consistent between the two studies is the AAS suppressed TBG and the consequent decline in total T4 and T3, and an increase in T3 resin uptake observed by Alen but not measured by Deyssig. Again, quoting from (2): “In relation to the changes in thyroid function parameters measured, we suggest that the primary target of androgen action was TBG biosynthesis.�

In a third study, this time performed by Malarkey et al in AAS-using females, the authors looked at Total T4, FreeT4, TSH, and TBG (4). The authors observed that


Thyroxine-binding proteins also were decreased in the steroid users, as reflected by the low thyroxine binding index and the decrease in total serum thyroxine levels. These latter changes had no significant influence on the biological activity of thyroid hormone, however, because the free thyroxine concentration and the thyroid stimulating hormone level were within normal limits. These findings are similar to those of a previous report of decreased thyroxine-binding globulin in men who were using anabolic steroids [2].

Note here though that while TSH was “within normal limits� it was nevertheless elevated significantly compared to controls (2.5 mU/L vs 0.8 mU/L).

The difference between this study and the previous one by Alen is that in (4) free T4 was unchanged, while in (2) there was a drop in free T4. Also here TSH was elevated in the AAS users while in Alen et al it was depressed. In the current study the combination of normal free T4 but elevated TSH is suggestive of subclinical hypothyroidism. However, to truly meet the criteria required for that diagnosis TSH would have to be elevated above 5.0 mU/L (although some physicians have argued that that threshold should be lowered). Technically, these subjects would be considered euthyroid (normal).

One criticism of the studies examined thus far is that in each case the subjects used a cocktail of anabolic steroids, including ones that aromatize and others that do not. Might there be a difference in the thyroidal effects of the two classes of drugs? A study by Lovejoy et al (5) addressed that question as part of research looking at the broader differences between the metabolic effects of oral (oxandrolone) and parenteral (testosterone) steroids. Lovejoy’s group administered each drug separately to groups of subjects. Testosterone aromatizes to estrogen, and estrogen has an opposite effect on TBG from pure androgens: the former elevates TBG while the latter lowers it. If the primary effects of AAS on measured thyroid parameters result from changes in TBG, then testosterone would be expected to have only a minor effect, the increased androgen and estrogen levels tending to cancel each other’s effects. Indeed this was the case in (5). Testosterone had no significant effect on any parameter measured (T4; TSH; T3 resin uptake; or free thyroxine index, a calculated measure of free T4).

Oxandrolone on the other hand does not aromatize. The oxandrolone group showed a significant decrease in T4 and T3 resin uptake, with no change in TSH. Referring to Table 1 above, we see that the combination of low T4 and low T3 resin uptake is characteristic of hypothyroidism. This is the conclusion the authors arrived at as well, that the oxandrolone group experienced mild hypothyroidism. Again, as in the study by Deyssig & Weissel, even though T4 and T3 resin uptake were low relative to placebo the values fell within the normal range, making the diagnosis of “hypothyroidism� a relative one rather than a clinical one. Clinically all subjects would be classified as euthyroid. And as in the other studies the authors here concluded “these changes were most likely due to the effects of sex steroids on thyroid binding globulin (TBG).� The authors also observed that the Free T4 Index was higher in the oxandrolone group than either the placebo or testosterone groups.

olddawg
06-11-2013, 05:55 PM
A recent study looked at the effects of short-term methyltestosterone administration to normal subjects (6). The researchers found that total T4, total T3, and TBG were lowered, as we have come to expect. However, TSH and free T4 were elevated as well compared to the subjects’ baseline values. Again all hormone values remained within the normal range. The authors speculate that the elevated TSH and free T4 could be due to increased sensitivity of the thyroid to TRH or decreased sensitivity to hormonal feedback, suggesting some form of mild impaired thyroid function. As with the study by Deyssig, if this functional impairment were real, it would be subclinical and of dubious relevance. Note also that the elevated TSH measured by Daly et al differs from the depressed TSH observed by Alen et al. Daly et al speculate that this may be due to the fact that they sampled blood after six days vs 4 weeks and longer in the study by Alen et al.

A 1984 study by Small et al examined the effects of 10 mg daily of stanozolol, another nonaromatizing steroid, for 14 days in nine healthy subjects (7). This dosage was enough to lower testosterone by 50% and LH by 30%. TBG, T4 and T3 were lowered significantly, with no change in free T4 or TSH. This is the “standard model� of action of androgens on thyroid parameters stressed in endocrinology texts: no change in thyroid function, merely a lowering of TBG with the expected lowering of total thyroid hormone levels, but no effect on the physiologically relevant free hormone levels. To quote from the study,

“The changes found in thyroid hormones are in accord with the well known effects of anabolic steroids on thyroid function tests. Both T3 and T4 fell as a result of the reductions in TBG levels. The lack of change in TSH or Free T4 indicates that important physiological changes of thyroid function do not occur during treatment with stanozolol.�


We can summarize the results of the studies for comparative purposes by tabulating the data in Fig 2.


T4 T3 TSH T3 resin uptake Free T4 TBG
Deyssig low low 0 - 0 low
Alen low low low high low low
Lovejoy (test) 0 - 0 0 0 -
Lovejoy (ox) low - 0 low high -
Malarkey low - high - 0 low
Daly low low high - high low
Small low low 0 - 0 low


Table 2. Summary of measured thyroid parameters ( 0, no change; - unmeasured; )

Fluoxymesterone at 10 mg per day caused the by now familiar drop in TBG and total thyroid hormone levels with no effect on free parameters (8). Quoting from this study,

“Fluoxymesterone administration was accompanied by a reduction in thyroid binding globulin (with associated decreases in T3 and increases in T3 resin uptake). The free T4 index was unaltered, which implies that thyroid function was unchanged.�

Thus far we have looked at studies involving humans. One study that is often cited in the bodybuilding literature as evidence that trenbolone in particular suppresses thyroid function was done in sheep (9). However, in this study only total T4 was measured, not free T4, so we cannot conclude from this research that bioavailable T3 was affected in any way.

Can we make any sense out of the seeming hodgepodge of conflicting data? The only parameters that are consistent from study to study, where they were measured, are depressed total T3 and T4, and TBG. As we have discussed, androgens typically lower TBG, along with total T4 and T3 since the latter are a function of TBG levels. This however does not necessarily reflect thyroid dysfunction since the physiologically significant free fractions of these hormones typically remain in the normal range. If TBG levels change rapidly, however, a period of disequilibrium will exist during which thyroid function will be perturbed. This could explain the low free T4 and TSH observed by Alen as follows: The abrupt drop in TBG leads to a drop in bound T4, but free T4 remains elevated. This causes a shift in hormone from the blood to tissues because of a steeper free T4 concentration gradient. This increases the degradation rate of hormone in peripheral tissues. The increased tissue concentration of T4 signals the pituitary to lower TSH production, which will be reflected by temporarily lowered free T4 until the appropriate thyroid hormone/TBG ratio, and plasma/tissue ratio is reestablished. Alen et al discuss this possibility, and the process is illustrated graphically here:


http://www.thyroidmanager.org/Chapter5/5a-frame.htm

In conclusion then AAS seem to have little if any effect on thyroid function per se. The reports by Deyssig & Weissel, and Daly et al suggest the possibility of a direct action of AAS on the thyroid or pituitary, but their results are inconsistent: The former researchers detected elevated stimulated TSH while the latter saw an increase in basal TSH. Free T4 was unchanged in former group, while it was elevated in the latter. The only consistently reported effect is a depression in total T4, total T3 and TBG. If there is a direct effect of AAS on the thyroid, pituitary, or hypothalamus the studies conducted so far shed little light on the mechanism due to their inconsistent results. And as stressed by Deyssig & Weissel any direct effect of anabolic steroids on the thyroid would likely be of no clinical significance due to its small magnitude.

From a practical standpoint for those concerned that anabolic steroids might suppress the thyroid it is a simple matter to incorporate low dose (25 to 50 mcg/day) T3 into a cycle to enhance fat loss while at the same time only minimally if it all compromising gains in muscle mass (10). In (10) one group of subjects was given T3 alone while the other was given a combination of T3 and testosterone enanthate, 200 mg/week. After 28 days of bed rest, the men in the T3 group lost an average of 3.9 kg of body weight (i.e. from 82.0 ± 7.1 to 78.1 ± 7.1 kg). Body weight in the T3 plus testosterone-treated subjects declined by only 1.0 kg (78.9 ± 4.9 to 77.9 ± 4.9 kg). Lean body mass declined by 1.5 kg in the T3 group, whereas the T3 plus testosterone-treated subjects experienced nearly a 2-kg increase in lean mass (i.e. 1.7 ± 0.9 kg). Of course we don’t know how much mass the test plus T3 group would have gained had they foregone the T3. Nevertheless these are still impressive gains considering the subjects were forced to lie in bed for 28 days with no exercise, and considering that no special dietary measures were imposed to preserve or increase muscle mass.



References:

(1) Deyssig R, Weissel M. Ingestion of androgenic-anabolic steroids induces mild thyroidal impairment in male body builders. J Clin Endocrinol Metab. 1993 Apr;76(4):1069-71

(2) Alen M, Rahkila P, Reinila M, Vihko R. Androgenic-anabolic steroid effects on serum thyroid, pituitary and steroid hormones in athletes. Am J Sports Med. 1987 Jul-Aug;15(4):357-61

(3) Lum SM, Nicoloff JT, Spencer CA, Kaptein EM Peripheral tissue mechanism for maintenance of serum triiodothyronine values in a thyroxine-deficient state in man. J Clin Invest. 1984 Feb;73(2):570-5.

(4) Malarkey WB, Strauss RH, Leizman DJ, Liggett M, Demers LM. Endocrine effects in female weight lifters who self-administer testosterone and anabolic steroids. Am J Obstet Gynecol. 1991 Nov;165(5 Pt 1):1385-90.

(5) Lovejoy JC, Bray GA, Greeson CS, Klemperer M, Morris J, Partington C, Tulley R. Oral anabolic steroid treatment, but not parenteral androgen treatment, decreases abdominal fat in obese, older men Int J Obes Relat Metab Disord. 1995 Sep;19(9):614-24.

(6) Daly RC, Su TP, Schmidt PJ, Pagliaro M, Pickar D, Rubinow DR. Neuroendocrine and behavioral effects of high-dose anabolic steroid administration in male normal volunteers. Psychoneuroendocrinology. 2003 Apr;28(3):317-31

(7) Small M, Beastall GH, Semple CG, Cowan RA, Forbes CD. Alteration of hormone levels in normal males given the anabolic steroid stanozolol. Clin Endocrinol (Oxf). 1984 Jul;21(1):49-55

(8) Spitz IM, Margalioth EJ, Yeger Y, Livshin Y, Zylber-Haran E, Shilo S. Effect of non aromatizable androgens on LHRH and TRH responses in primary testicular failure. Horm Metab Res. 1984 Sep;16(9):492-7.

(9) Donaldson IA, Hart IC, Heitzman RJ. Growth hormone, insulin, prolactin and total thyroxine in the plasma of sheep implanted with the anabolic steroid trenbolone acetate alone or with oestradiol. Res Vet Sci. 1981 Jan;30(1):7-13.

(10) Zachwieja JJ, Smith SR, Lovejoy JC, Rood JC, Windhauser MM, Bray GA. Testosterone administration preserves protein balance but not muscle strength during 28 days of bed rest. J Clin Endocrinol Metab. 1999 Jan;84(1):207-12.

Jelisej
06-12-2013, 03:41 AM
Interesting topic, from my own research/experience- I would say that different AAS have different effect on thyroid, neverthless they do have an effect otherwise I beleive that AAS would have far less of an effect than they do.
Funny thing is that even people who agree that AAS have an effect dont really agree on anything else

this is text of Patrick Arnold:
ANABOLIC STEROID USAGE AND THYROID SUPPRESSION
Patrick Arnold

[...]

Bodybuilders who use large amounts of anabolic steroids often report lethargy as a side effect. Sleepiness, irritability, and foggy-headness are commonly reported by users of some of the more powerful anabolic steroids in large dosages. The cause of this lethargy has been the subject of debate in the performance-enhancement drug community, and the solution may be multifactorial. Published studies have given reason to suspect that thyroid hormone suppression may be one of these factors.

THYROID HORMONES

There are two major thyroid hormones, T4 and T3. T3 is considered the most active thyroid hormone, and its job is to act as a sort of ter regulator of every major aspect of metabolism- from protein thesis to carbohydrate and fat oxidation. T3 acts in general as a metabolic stimulator, and in addition to its influence on how the uses fuel for energy and tissue building, it also works to generate heat production (thermogenesis) via enhancement of uncoupling protein 1 (UCP-1) expression in the liver.

The production of too much thyroid hormone (hyperthyroidism) and too little thyroid hormone (hypothyroidism) are both undesirable conditions. Hyperthyroidism leads to overstimulation of the nervous system (resulting in elevated heart rate and nervousness), as well loss of lean body mass due to protein catabolism. Hypothyroidism; the other hand, leads to depression and fatigue, as well as other symptoms such as joint pain, sensitivity to cold, and fat gain.

ANABOLIC STEROIDS AND THYROID SUPPRESSION

As I stated in my introduction, published studies have confirmed that anabolic steroid use can suppress thyroid hormone levels in the blood. It appears that this is not due so much to a decrease in the production of the main thyroid hormone (T4) in the thyroid gland, however. What really is the culprit of the suppression is debatable, as different studies have found different things. Two things are clear, though. The levels of total and free active thyroid hormone (T3) are decreased with anabolic steroid use, and T4 thyroid hormone-binding globulin levels are markedly elevated. However, free T4 appears to be unchanged, as does TSH, which is the hormone that your brain produces to stimulate thyroid hormone production in the thyroid gland. So what is happening is not entirely clear. It may be a combination of disrupted conversion of T4 to T3 and/or interference of bioavailable T4 levels by excessive T4 thyroid hormone-binding globulin. Whatever the case, levels of the active thyroid hormoneT3 can be suppressed by anabolic steroid use- particularly at higher dosages. Such suppression can interfere with maximum muscle growth from a cycle, as optimal protein synthesis activity is dependent upon ideal T3 levels in the body.

It is interesting to note that bodybuilders have discovered by trial and error that thyroid hormone supplementation leads to greater gains during a cycle. I am pretty sure that this anecdotal discovery was made without the knowledge that AAS (anabolic-androgenic steroid) usage is thyroid suppressive.

Psychoneuroendocrinology. 2003 Apr;28(3):317-31. Related Articles, Links


Neuroendocrine and behavioral effects of high-dose anabolic steroid administration in male normal volunteers.

Daly RC, Su TP, Schmidt PJ, Pagliaro M, Pickar D, Rubinow DR.

Behavioural Endocrinology Branch, National Institute of Mental Health, Building 10, Room 3N238, 10 Center Drive MSC 1277, Bethesda, MD 20892-1277, USA. dalyr@intra.nimh.nih.gov

OBJECTIVE: Despite widespread abuse of anabolic-androgenic steroids (AAS), the endocrine effects of supraphysiologic doses of these compounds remain unclear. We administered the AAS methyltestosterone (MT) to 20 normal volunteers in an in-patient setting, examined its effects on levels of pituitary-gonadal, -thyroid, and -adrenal hormones, and examined potential relationships between endocrine changes and MT-induced psychological symptoms. METHOD: Subjects received MT (three days of 40 mg/day, then three days of 240 mg/day) or placebo in a fixed sequence with neither subjects nor raters aware of order. Samples were obtained at the ends of the baseline, high-dose MT and withdrawal phases. Potential relationships between hormonal changes and visual analog scale measured mood changes were examined. RESULTS: Significant decreases in plasma levels of gonadotropins, gonadal steroids, sex hormone binding globulin, free T3 and T4, and thyroid binding globulin (Bonferroni t, p<0.01 for each) were seen during high-dose MT; free thyroxine and TSH increased during high-dose MT, with TSH increases reaching significance during withdrawal. No significant changes in pituitary-adrenal hormones were observed. Changes in free thyroxine significantly correlated with changes in aggressiveness (anger, violent feelings, irritability) (r=0.5,p=0.02) and changes in total testosterone correlated significantly with changes in cognitive cluster symptoms (forgetfulness, distractibility) (r=0.52,p=0.02). Hormonal changes did not correlate with plasma MT levels. CONCLUSIONS: Acute high-dose MT administration acutely suppresses the reproductive axis and significantly impacts thyroid axis balance without a consistent effect on pituitary-adrenal hormones. Mood and behavioral effects observed during AAS use may in part reflect secondary hormonal changes.

Publication Types:
Clinical Trial
PMID: 12573299 [PubMed - indexed for MEDLINE]
J Clin Endocrinol Metab. 1993 Apr;76(4):1069-71. Related Articles, Links


Androgenic-anabolic steroid effects ... [Am J Sports Med. 1987 Jul-Aug] - PubMed - NCBI (http://www.ncbi.nlm.nih.gov/pubmed/3661817)

http://psy2.ucsd.edu/~mgorman/Daly.pdf

This is a good (and long) read, which is not directly talking about AAS but logicaly you will draw conclusion that AAS have an impact on thyroid:
http://icb.oxfordjournals.org/content/37/2/185.full.pdf

olddawg
06-12-2013, 04:43 AM
Being hypothyroid, I am on rx meds for it. I can tell that on tren so far of all the aas that my thyroid slows in spite of the meds to keep it working properly. Bloods have confirmed it. Doc is always baffled after a tren cycle bloods --of my slow thyroid and always asks me to take the eltroxin with no calcium. I get a little giggle inside cause I know why the bloods are what they are. So it's pretty obvious to me that tren will slow the thyroid

BoneDaddy
06-12-2013, 05:36 AM
So should we be adding 50mcg of T3 to cycles? Thyroid friendly supps PCT and/or during sound good right about now, too........

Jelisej
06-12-2013, 05:53 AM
Being hypothyroid, I am on rx meds for it. I can tell that on tren so far of all the aas that my thyroid slows in spite of the meds to keep it working properly. Bloods have confirmed it. Doc is always baffled after a tren cycle bloods --of my slow thyroid and always asks me to take the eltroxin with no calcium. I get a little giggle inside cause I know why the bloods are what they are. So it's pretty obvious to me that tren will slow the thyroid

Things that I'm 100% sure is:
Testosterone itself can have depressing effect on TSH so in long run (TRT for example) it can reduce levels of thyroid hormones so lot of people on TRT end up adding thyroid hormones to their regimen,
HGH on other hand increases T4-T3 conversion, so people may end up with depleted T4-

also few times I've seen some bloodworks but they are bit inconclusive- anyway- I think vast majority of AAS/Ph's will not cause permanent damage to thyroid, but if there are underlying issues they will come to surface- I would compare it to the effect of AAS on hairloss.

Also I would say that for majority of cycles adding soem thyroid hormones would be benefitial regarding gains BUT I would strongly suggest not to do that as its shown that use of thyroid hormones (I think its T3 but not sure) can permanently elevate SHBG levels, which is not a good thing at all.
Again looking at the organ itself- thyroid is not like HPTA and it will allow you to "top up" hormone levels freely to reach youthfull levels without any supression, and there is enough data and from my own experience (and few other folks) I would say that even if there is "shutdown" thyroid will restore its function within week-or-two.
But again most likely it will make SHBG levels go up permanently, which will bind lot of hormones and effectively you'll become hypogonadal even with good TT levels.
Other thing is too much T3 will cause elevated reverseT3 which has its own troubles.

olddawg
06-12-2013, 06:20 AM
fucking complicated! My feeling is that on a cut you may want to address your thyroid's performance as metabolism is everything, so adding something in for it "might" be a good idea. On a bulk or recomp, I'd just let it drop if it does and then recover afterward to avoid further complicating things.

Jelisej
06-12-2013, 06:34 AM
fucking complicated! My feeling is that on a cut you may want to address your thyroid's performance as metabolism is everything, so adding something in for it "might" be a good idea. On a bulk or recomp, I'd just let it drop if it does and then recover afterward to avoid further complicating things.

Bulk or cut you need thyroid hormones, "cut" part is well known, bulk is similar- faster matabolism- more hormone used, basically uptake in cell will be increased.
For example if we compare person with higher thyroid hormones and lower tt levels (lets say 600 ng/dl) and one with lower thyroid and higher tt levels (lets say 800 ng/dl)- person with 600 ng/dl will have more benefits as more of it is being used, basically he is running in the higher gear.
So its like comparing two cars one is running in 3 (third) gear with maximum acceleration and one in 5 with medium acceleration; which one is likely to go faster?

olddawg
06-12-2013, 07:09 AM
I give up, which one? lol

the faster the thyroid the more catabolism though --no?

Rodja
06-12-2013, 07:46 AM
I give up, which one? lol

the faster the thyroid the more catabolism though --no?

Potentially. It's a somewhat common practice to use a low-dose of T3 on-cycle to increase protein utilization.

BoneDaddy
06-12-2013, 08:06 AM
Fascinating read, fellas.

Jelisej
06-12-2013, 04:22 PM
I give up, which one? lol
the faster the thyroid the more catabolism though --no?

Yes, unless you become more anabolic (lol)- let me explain you from TRT perspective- one starts T shots, his tt levels go up (lets say that at this point person is anabolic) which makes thyroid hormones to be "spent" and (also adrenals), because testosterone is being used a lot total/free testostosterone level goes down (at this point person may become "catabolic") so now one increases testosterone dosage (and probably becomes anabolic again) now thyroid level drops down again -possibly at this point thyroid may not be able to cope anymore so he adds some thyroid hormones (and probably some adrenal support) at this point his metabolic rate is quite fast and because of thyroid meds his SHBG is up- so persons free test is low- he ads some more testosterone to overrun SHBG and top up his free testosterone- he is anabolic again and his free test is high and so is total test (maybe little bit maybe a lot), and he feels darn good.

olddawg
06-12-2013, 05:17 PM
ha ha bonedaddy nice avi.
so jj, over how long of a timeframe would these changes happen say every 2 weeks or so?

Jelisej
06-12-2013, 05:46 PM
Well on TRT would be different, it takes couple weeks for thyroid to level up, obviously one cannot afford that on cycle so basically one can add 25 mg (with possibility to increase up to 50 mg of T3 insome cases)- (IMO best option is to use T3 in pyramide style- start with 12.5 and than increase and vice versa) - but probably its best to stay away from T3 as I said before it can possibly cause permanently elevated SHBG levels, so probably is best to do shorter cycles for which persons natural levels should suffice.

In your case as you are already on thyroid meds you can feel free to use T3- but best would be to sort out your thyroid protocol first and then just add bit more when on cycle.

Other thing is T3 may not agree with some compounds.

olddawg
06-12-2013, 06:05 PM
thanks, yeah I won't mess with my thyroid dose. I have lots of other options I can use first --slin, gh, aas combos still so I won't adjust it. just trying to get my head around it.

olddawg
06-12-2013, 07:13 PM
thanks jj, i'm gonna talk to the doc in just about 8 weeks when I get bloods about the t3. and you mean 25mg t3 while on cycle not t4 right? My doc is reluctant but not too bad. she has given me lisinopril for bp while on cycle, it's prescribed as needed with unlimited refills. I told her either I ordered it from India, or she gave me a script. I think she made a good choice with my health in mind

BoneDaddy
06-12-2013, 07:24 PM
ha ha bonedaddy nice avi.


I need it for motivation!

Jelisej
06-13-2013, 06:22 AM
thanks jj, i'm gonna talk to the doc in just about 8 weeks when I get bloods about the t3. and you mean 25mg t3 while on cycle not t4 right? My doc is reluctant but not too bad. she has given me lisinopril for bp while on cycle, it's prescribed as needed with unlimited refills. I told her either I ordered it from India, or she gave me a script. I think she made a good choice with my health in mind

Yes T3 is what is needed for most cycles, one of the exception would be HGH.
And yes T3 will be great addition to your regimen, lot of people who were on T4 only had improvement when adding T3 on top.

burlyman30
06-13-2013, 07:54 AM
And yes T3 will be great addition to your regimen, lot of people who were on T4 only had improvement when adding T3 on top.

Makes me wonder why Armour thyroid is not used as a more standard treatment.

olddawg
06-13-2013, 09:06 AM
I'm actually going to have to research pretty thoroughly and print off some info for my doc. likely she is not up on either of them or else she'd already be prescribing them to me.

and JJ every time I see your avi I think of the rock!

h2s
06-13-2013, 09:34 AM
Some good info in this thread.

Jelisej
06-13-2013, 03:56 PM
Makes me wonder why Armour thyroid is not used as a more standard treatment.

It has too much T3 compared to T4 (for majority of folks), so what people do they combine Armour thyroid with some T4.
Also some people complain about inconsistency, so for some people who are sensitive find it hard to dose. Most of doctors avoid it for these reasons.
Combining with T4 works fine for majority of folks, also some say that it has advantage over synthetic drugs as it contains T2 and T1m though some endos say that brain can convert synthetic ones, I think it goes T4>T3>T2>T1

Other product similar is natural sources raw thyroid, which has a good reputation but is not good with folks with hashimoto.

Jelisej
06-13-2013, 03:59 PM
I'm actually going to have to research pretty thoroughly and print off some info for my doc. likely she is not up on either of them or else she'd already be prescribing them to me.

and JJ every time I see your avi I think of the rock!

I love rock.

Check out this site and show it to your doc:
Stop the Thyroid Madness - Hypothyroidism and thyroid mistreatment (http://www.stopthethyroidmadness.com/)
It has a lot of good info, maybe they are pushing T3 bit too much- but other than that I would say lot of decent info, most of things is confirmed "in a field".

Jelisej
06-13-2013, 04:32 PM
Optimising thyroid naturaly

1. Preload selenium for couple of weeks up to 400 mcg
2. Add iodine* (lugol has a good reputation and iodoral is not bad) not sure about max dosage
3.Add l-tyrosine (mind you that l-tyrosine can convert to dopamine and also norepinephrine, and if it goes too much to norepinephrine person may feel jittery, restless) 1-2 grams
4. Also add Vitamin B6 (as pyridoxal 5’-phosphate) 100mcg
5. Some say its good to add Tryptophan (up to 2gr)- at night to "calm down" if there are issues from l-tyrosine


Generaly people take iodine well, but people with hashimoto have an issues, but apparently if one is preloading selenium then there should be no problem- I cannot confirm this, anyway here is an article by Jeffrey Dach who also claims that preloading selenium prevents issues with iodine:
Jeffrey Dach MD Bio-Identical Hormone Blog: Iodine is Safe and Effective by Jeffrey Dach MD (http://jeffreydach.com/2011/04/06/iodine-is-safe-and-effective-by-jeffrey-dach-md.aspx)

olddawg
06-13-2013, 08:01 PM
You must spread some Reputation around before giving it to Jelisej again. Too bad we couldn't buy you a lap dance jj,

pman42
06-13-2013, 10:15 PM
Hmm, I was under the impression that once a person went on thyroid meds it was hard to discontinue them. Jelisej, you're saying that the thyroid responds well to "topping up" without suppressing it. Mind if I ask where you got this from?

iodine is kinda a weird one. I was told by one of my teachers, an ND, that over 800mcg a day can suppress thyroid function. yet many people around the world routinely consume WAY over this amount from seaweeds.

Jelisej
06-14-2013, 06:02 AM
Hmm, I was under the impression that once a person went on thyroid meds it was hard to discontinue them. Jelisej, you're saying that the thyroid responds well to "topping up" without suppressing it. Mind if I ask where you got this from?

iodine is kinda a weird one. I was told by one of my teachers, an ND, that over 800mcg a day can suppress thyroid function. yet many people around the world routinely consume WAY over this amount from seaweeds.

I've seen some bloodworks, plus personal experience- my thyroid was sluggish so I was doing some "tests"- I used 25mg of T3 and 50mg of T4, I did not do bloods after, but going by the symptoms- after cesation I felt it for 3 days after that situation returned to "normal".
But dont get wrong idea- using T3 when you dont need it is asking for trouble, and using it for losing weight is double edge sword.

Also there were some research somewhere about people who were (wrongly) put on thyroid meds and after years being on meds they thyroid function was restored back to normal.

99.99% of thyroid diseases is caused by auto-immune diseases, basicaly our own body attacks thyroid and there are no known cures for that, it can only be slowed down and symptoms alleviated- so basically thyroid treatment is for life because of those reasons.