HYPOTHYRODISM from T3 --> Help !!!!

[junk]

Gee Nadi thanks for the abstruct. Now I'm even MORE confused

Fonz say: stay away from ECA, CLEN and other stimulants, and you are actually showing a proof that ECA may help me recover. I've also read a lot of other places not to touch Ephedrive or Caffeine in situations like myself. But you're stating an interesting research. Maybe I will go for it

 

[nandi12]

When people say to avoid adrenergic agonists like ephedrine while your thyroid is recovering, their concern I believe is that the elevated T3 will act in a negative feedback way to slow thyroid recovery. This is a valid concern, although it is a hypothesis rather than someting that has been shown to actually occur.

As I suggested, just giving your thyroid a little more time is probably the best strategy. However, it sounds like you are suffering miserably from your symptoms. So you have a decision. You could supplement with ephedrine which will raise your metabolic rate and improve your symptoms with a POSSIBILITY of the elevated T3 slowing complete recovery. Or you can live with the symptoms longer and hope that your condition improves.

This is reflective of the division in the medical community about treating subclinical hypothyroidism: do you treat the symtoms even when thyroid function is normal (as yours appears to be according to the numbers), or do you withold treatment out of concern for side effects.

It is a complicated issue.


www.cuttingedgemuscle.com

 

[Fonz]

I'd give myself a bit more time to recover. I seriously doubt the T3 permanently damaged your thyroid. Without knowing your free T3 it is impossible to tell (as far as I know) whether you are having a problem converting the T4 into T3.

There is an argument in the medical community over just how common is the problem of a low rate of conversion of T4 to T3. The majority of doctors probably believe "Wilson's Syndrome" is not real, others believe it is very real and quite common. The problem is compounded by the fact that the majority of people who complain of being hypothyroid yet show normal thyroid results are women. Unfortunately doctors are known to tell female patients that "it is all in your head" when they present with a problem the doctor can't solve.

There is also a division in the medical community about whether low dose thyroid hormone should be given to patients who have "subclinical hypothyroidism". These people usually present with a high normal TSH and normal hormone levels, but complain of hypothyroid symptoms. Again, since the majority are women, they are often not given thyroid hormones. My wife is in this group. The docs kept saying "you're normal" and would not prescribe T3 or T4. So she just started treating herself and now she fells 100% better. (Not that this is your problem though because your TSH is low normal)

You could try an ECA stack to boost metabolism. Ephedrine used for a short period (a few weeks) enhances the conversion of T4 to T3 (1). If you started feeling better it would suggest that conversion might be your problem.

In any case, I hope you start feeling better soon.

(1) Am J Clin Nutr 1985 Jul;42(1):83-94

Enhanced thermogenic responsiveness during chronic ephedrine treatment in man.

Astrup A, Lundsgaard C, Madsen J, Christensen NJ.

The thermogenic effect of a single oral dose of ephedrine (1 mg/kg body weight) was studied by indirect calorimetry in five women with 14% overweight before, during and 2 mo after 3 mo of chronic ephedrine treatment (20 mg, perorally, three times daily). Before treatment and 2 mo after its cessation a similar thermogenic response to ephedrine was observed. The total extra consumption of oxygen was 1.3 1 before and 1.2 1 after cessation of the chronic treatment. After 4 and 12 wk of treatment ephedrine elicited a more sustained response, the extra oxygen consumption in the 3 h following ephedrine intake being 7.0 and 6.9 1, respectively. The ratio of serum T3 to T4 increased significantly after 4 wk of treatment (15.6 +/- 1.3 vs 19.4 +/- 2.4; p less than 0.05), but decreased below the initial value after 12 wk treatment. The mean body weight was significantly reduced after 4 and 12 wk of treatment (2.5 and 5.5 kg, respectively). An improved capacity for beta-adrenergic induced thermogenesis may be useful in the treatment of obesity.

One problem Nandi. These were normal people w/ normal thyroid function, not downregulated.

If he took ECA, T4 would not be converted to T3, but more than likely the metbolically inactive reverse T3(rT3).

I don't think it is a good time to use any kind of stimulant that mimics adrenaline in any way, and targets the SNS. He wants the SNS system to recover......along w/ his thyroid function. These two as you well know are interrelated.

Best bet, is to use a Dopamine Agonist such as Bromocriptine which targets the PNS.

He will be getting its appetite suppressant effects plus his thyroid gland and his SNS will be allowed to recover.

Fonz

 

[junk]

Thanks Fonz, can you please (This will be last answer these question for me:

* I didn't know Clen had any bad property on the Thyroid. I thought this was only with NYC and ECA not with Clen. But if you say so I take it. Thing is I didn't want to fucking loose everything I've worked for so hard in the gym. But you're the guru.


* MOST IMPORTANT Question: Do you think I should still go on with a very low caloric diet (about 1700 cals) along with 60 minutes (@70voMax) cardio every morning and 3 times a week weight-training?
I mean, I should do whatever I can to speed up metabolism right? But it will also probably kill all my muscle tissues completely because I've just finished my cutting cycle and started clomid. So I am lost here.
Don't forget that I'm just POST cutting cycle and began Clomid therapy a few days ago. This would be the worest time to make long session cardios, wait an hor before eating and only eat 1500-1700 cals a day, don't you think?

 

[nandi12]

If he took ECA, T4 would not be converted to T3, but more than likely the metbolically inactive reverse T3(rT3).

There are two problems, Fonz.

First, can you document from the scientific literature that the statement in quotations is true?

Second, according to his thyroid test, his hormone values (TSH and fT4) ARE normal, not depressed. His low total T3 does not mean anything necessarily because he has been using AAS, which lower total thyroid hormone values.

This situation is analogous to the one described in the abstract below. These doctors had to treat this guys AAS induced hypogonadism. First, they alleviated the symtoms by giving him sustanon. Then they treated the hypogonadism with HCG. They could just as easily withheld the sustanon and used onlyHCG, probably speeding his recovery, but prolonging his misery.

People are always looking for black and white answers. Often there aren't any.

Postgrad Med J 1998 Jan;74(867):45-6

Anabolic steroid induced hypogonadism treated with human chorionic gonadotropin.

Gill GV.

Endocrine Unit, Walton Hospital, Liverpool, UK.

A case is presented of a young competitive body-builder who abused anabolic steroid drugs and developed profound symptomatic hypogonadotrophic hypogonadism. With the help of prescribed testosterone (Sustanon) he stopped taking anabolic drugs, and later stopped Sustanon also. Hypogonadism returned, but was successfully treated with weekly injections of human chorionic gonadotropin for three months. Testicular function remained normal thereafter on no treatment. The use of human chorionic gonadotropin should be considered in prolonged hypogonadotrophic hypogonadism due to anabolic steroid abuse

 

[nandi12]

I didn't know Clen had any bad property on the Thyroid

To answer your question, clen has basically the same effect as ephedrine: it increases the peripheral conversion of T4 to T3

Clin Endocrinol Metab 1984 May;58(5):895-903

Effects of chronic beta-receptor stimulation on sympathetic nervous system activity, energy expenditure, and thyroid hormones.

Scheidegger K, O'Connell M, Robbins DC, Danforth E Jr.

The effects of hyper- and hypothyroidism on sympathetic nervous system activity and energy expenditure are well recognized. The impact of altered sympathetic nervous system activity on energy expenditure and thyroid hormone metabolism has not been well studied. We investigated the effects of orally administered terbutaline sulfate, a beta 2-receptor agonist (5 mg, three times per day for 2 weeks), on the activity of the sympathetic nervous system, energy expenditure, and thyroid hormone metabolism in six normal men, aged 21-36 yr. The cardiovascular, metabolic, and thermogenic responses to an infusion of the beta-adrenergic agonist isoproterenol were clearly blunted after 2 weeks of treatment with terbutaline sulfate, indicating down-regulation of beta-receptors and/or development of reduced sensitivity. There were no significant changes in the cardiovascular, metabolic, or thermogenic responses to an infusion of the alpha-adrenergic agonist phenylephrine. Basal metabolic rate was significantly increased by the chronic administration of terbutaline sulfate [5.040 +/- 0.167 (+/- SE) vs. 5.421 +/- 0.234 kJ/min; P less than 0.05]. There was a highly significant change in the serum T3 to T4 ratio (19.4 +/- 1.0 vs. 24.4 +/- 1.0; P less than 0.001). This was a result of increased serum T3 concentrations (136 +/- 9 vs. 160 +/- 14 ng/dl; P less than 0.05) and decreased serum T4 concentrations (7.2 +/- 0.8 vs. 6.7 +/- 0.8 micrograms/dl; P = NS). Chronic beta-receptor stimulation with terbutaline sulfate increases the basal metabolic rate and T3 concentrations. These changes occurred despite down-regulation of beta-receptors and/or decreased sensitivity in response to chronic terbutaline administration.

Also, the LAST thing you would want to take is bromocriptine. Bromocriptine has been used successfully to treat HYPERTHYROIDISM not hypothyroidism. A number of studies like the one below have shown that dopaminergic agonists lower TSH levels. This is the opposite of what you are trying to achieve:

J Clin Endocrinol Metab 1984 May;58(5):934-6

Bromocriptine therapy for hyperthyroidism due to increased thyrotropin secretion.

Takamatsu J, Mozai T, Kuma K.

We describe a patient with TSH-induced hyperthyroidism successfully treated with bromocriptine. A 25-yr-old woman was found to have hyperthyroidism due to excessive TSH secretion; no pituitary tumor was found. Her serum T4 level ranged between 21.9 and 25.9 micrograms/dl and that of T3 between 283 and 314 ng/dl. Serum TSH was between 5 and 9 microU/ml with an exaggerated response to TRH. Basal metabolic rate was +26 to +38%. Serum PRL was also elevated (79 ng/ml). Administration of bromocriptine for 4 months decreased serum TSH and PRL levels to normal with a concomitant fall in levels of serum T3 and T4. Regression of the clinical manifestations of hyperthyroidism occurred during bromocriptine drug therapy. These results suggest that reduction in hypothalamic dopaminergic tone may have contributed to the inappropriately increased TSH secretion in the patient.

Further, to quote from an invitro study

"Dopamine (DA) and the dopaminergic agonists bromocriptine and apomorphine inhibit the secretion of TSH as well as that of PRL by rat anterior pituitary (AP) cells in monolayer culture... It is concluded that the dopaminergic stimulus causing the inhibition of TSH and PRL secretion from rat AP cells in culture is mediated via a high affinity DA receptor present upon lactotrophs and thyrotrophs and that this receptor has similar characteristics on the two cell types." (1)

(1) Endocrinology 1983 May;112(5):1567-77

Dopamine receptors on intact anterior pituitary cells in culture: functional association with the inhibition of prolactin and thyrotropin.

Foord SM, Peters JR, Dieguez C, Scanlon MF, Hall R.

 

[Fonz]

There are two problems, Fonz.

First, can you document from the scientific literature that the statement in quotations is true?

Second, according to his thyroid test, his hormone values (TSH and fT4) ARE normal, not depressed. His low total T3 does not mean anything necessarily because he has been using AAS, which lower total thyroid hormone values.

This situation is analogous to the one described in the abstract below. These doctors had to treat this guys AAS induced hypogonadism. First, they alleviated the symtoms by giving him sustanon. Then they treated the hypogonadism with HCG. They could just as easily withheld the sustanon and used onlyHCG, probably speeding his recovery, but prolonging his misery.

People are always looking for black and white answers. Often there aren't any.

Postgrad Med J 1998 Jan;74(867):45-6

Anabolic steroid induced hypogonadism treated with human chorionic gonadotropin.

Gill GV.

Endocrine Unit, Walton Hospital, Liverpool, UK.

A case is presented of a young competitive body-builder who abused anabolic steroid drugs and developed profound symptomatic hypogonadotrophic hypogonadism. With the help of prescribed testosterone (Sustanon) he stopped taking anabolic drugs, and later stopped Sustanon also. Hypogonadism returned, but was successfully treated with weekly injections of human chorionic gonadotropin for three months. Testicular function remained normal thereafter on no treatment. The use of human chorionic gonadotropin should be considered in prolonged hypogonadotrophic hypogonadism due to anabolic steroid abuse

If he goes into a hypocaloric diet right now, he is going to run into problems.
I'll explain why:


1: Endocrinol Metab Clin North Am 2002 Mar;31(1):173-89 Related Articles, Links


Effect of obesity and starvation on thyroid hormone, growth hormone, and cortisol secretion.

Douyon L, Schteingart DE.

Division of Endocrinology and Metabolism, Department of Internal Medicine, University of Michigan Medical School, 1150 West Medical Center Dr., Ann Arbor, MI 48109, USA.

Obesity and starvation have opposing affects on normal physiology and are associated with adaptive changes in hormone secretion. The effects of obesity and starvation on thyroid hormone, GH, and cortisol secretion are summarized in Table 1. Although hypothyroidism is associated with some weight gain, surveys of obese individuals show that less than 10% are hypothyroid. Discrepancies have been reported in some studies, but in untreated obesity, total and free T4, total and free T3, TSH levels, and the TSH response to TRH are normal.

(Check

Some reports suggest an increase in total T3 and decrease in rT3 induced by overfeeding. Treatment of obesity with hypocaloric diets causes changes in thyroid function that resemble sick euthyroid syndrome. Changes consist of a decrease in total T4 and total and free T3 with a corresponding increase in rT3.

(Done

untreated obesity is also associated with low GH levels; however, levels of IGF-1 are normal. GH-binding protein levels are increased and the GH response to GHRH is decreased. These changes are reversed by drastic weight reduction. Cortisol levels are abnormal in people with abdominal obesity who exhibit an increase in urinary free cortisol but exhibit normal or decreased serum cortisol and normal ACTH levels. These changes are explained by an increase in cortisol clearance. There is also an increased response to CRH. Treatment of obesity with very low calorie diets causes a decrease in serum cortisol explained by a decrease in cortisol-binding proteins. The increase in cortisol secretion seen in patients with abdominal obesity may contribute to the metabolic syndrome (insulin resistance, glucose intolerance, dyslipidemia, and hypertension).

(Check

States of chronic starvation such as seen in anorexia nervosa are also associated with changes in thyroid hormone, GH, and cortisol secretion. There is a decrease in total and free T4 and T3, and an increase in rT3 similar to findings in sick euthyroid syndrome.

(Done

The TSH response to TRH is diminished and, in severe cases, thyroid-binding protein levels are decreased. In regards to GH, there is an increase in GH secretion with a decrease in IGF-1 levels. GH responses to GHRH are increased. The [table: see text] changes in cortisol secretion in patients with anorexia nervosa resemble depression. They present with increased urinary free cortisol and serum cortisol levels but without changes in ACTH levels. In contrast to the findings observed in obesity, the ACTH response to CRH is suppressed, suggesting an increased secretion of CRH. The endocrine changes observed in obesity and starvation may complicate the diagnosis of primary endocrine diseases. The increase in cortisol secretion in obesity needs to be distinguished from Cushing's syndrome, the decrease in thyroid hormone levels in anorexia nervosa needs to be distinguished from secondary hypothyroidism, and the increase in cortisol secretion observed in anorexia nervosa requires a differential diagnosis with primary depressive disorder.

Publication Types:
Review
Review, Tutorial

PMID: 12055988 [PubMed - indexed for MEDLINE]



Hypocaloric diets actually see More T4 being converted into the metabolically active rT3(Reverse T3), than the mnetabolically active T3.
That is EXACTLY what he doesn't want right now.

He needs to bump up caloric intake to maintenace levels, so that more T3 is converted from T4......no rT3 as I have previously stated.
Combine this with a dopamine agonist such as bromo, and his recovery should be on its way.

Fonz

 

[Triple J]

This is a great thread.

Here is some conjecture based on my observations - if stimulants like ECA cause you to feel cold vs. warm, and you get deca dick like symptoms, this is probably a clue that they are impacting your thyroid and perhaps subsequent prolactin levels in a negative way.

Gurus please confirm if this makes sense to you.

 

[nandi12]

Here is some conjecture based on my observations - if stimulants like ECA cause you to feel cold vs. warm, and you get deca dick like symptoms, this is probably a clue that they are impacting your thyroid and perhaps subsequent prolactin levels in a negative way.

I think you are confusing the adrenergic effects of ephedrine (fight of flight type effects) like piloerection (goose pimples), shrivled up dick (ever try to get it up on amphetamines?), etc with thyroid and prolactin effects.

BTW, I agree 100% Fonz that he needs to maintain an isocaloric diet to ensure T4 to T3 conversion. But a person can still bump up their metabolic rate with ECA and maintain an isocaloric state. They just have to eat more.