don't be so contradictory
Here is my situation:
I did a cycle of steroids for about 10 weeks which ended in mid February. I used 25-50 mcg T3/day on that cycle. After the cycle, I experienced signs of thyroid shutdown such as freezing at night, but I didn’t get bloodwork. Over a few months, I slowly improved.
I’ve been cutting for the last 6 weeks. The first three weeks, I used ~40 mcg T3/day and the last three I used 50 mcg T4 and 2 iu GH/day. I’ve also used a mild cortisol blocker branded Lean Xtreme off and on the last few days. The lack of cortisol killed my ability to recover and sleep well. My BG was 61 this morning about 90 minutes after breakfast. To top it off, I haven’t really lost much fat on this cut.
I stopped the drugs today, and I want to get a complete metabolic panel, liver panel, thyroid panel, and total testosterone count. I know I need to wait sometime for the T4 to clear. How long should I wait, and what should I take/do in the meantime for optimal hormonal health? I’ve seen the recommendations in musclepump’s thread about his low T value and I take a lot of those supps and plan to take Premier Lab Raw Thyroid Extract,--although I don’t know what dose to take. Any advice is appreciated.
Last edited by Pirate!; 07-15-2006 at 01:56 PM.
don't be so contradictory
Martin's correct, you've jacked your cortisol around and now its pathway is depleted.
Best to use adaptogens rather than cortisol enhancers (like whole licorice root).
Adaptogens such as ashwaganda, Rhodiola rosea. Reishi (a mushroom), Chinese and American or Siberian ginseng and cordyceps would be best for you to use, Pirate, as you wait for your system to recover.
If your blood glucose was 61 less than two hours postparandial, you have severe hypoglycemia, a product of carb loading secondary to thyroid rebound.
That practice is also well known for causing glycogen loss from liver. It will take you, sir, a minimum of three solid months of careful eating to restore and replenish that dysfunctional glycogen storage mechanism.
You fuck with your thyroid, you damage its communication with adrenals and liver, and that, sends its desparate message to brain, to close a very destructive loop. In most cases, over time, it will naturally right itself. In some however, sufficient negative negative regulatory karma is built up, that the setpoint is altered. Without help, it sits idling, waiting for permission to exhale...
After a few more readings, it does appear that I'm consistently hypo. However, the IGFs from the GH likely contributed to this, and now that I'm off the GH I expect improvement in this area rather soon. I'll go ahead and get a thyroid panel done to assess T-3 Uptake, T4, T7, & TSH pretty soon. My thyroid med use hasn't been too extreme relative to what others are doing. I currently take Rhodiola rosea, and I will get some other adaptogens as well. That sounds like exactly what I need.
As for diet, I'll aim to eat at maintenance with whole grains, veggies, lean protein, and plenty of MUFAs.
I appreciate all your advice, Trouble. I'll update you on my lab results and progress over time.
Here is the adaptogen product I'm considering taking. Can you recommend a particular dose?
LOL, there is a recommended dosage at the bottom of that product content information.
I have no idea of the relative strength of their herbal sources. It would be foolish for me to recommend anything other than the recommended dosage.
I find it a bit odd that everything is present in equal proportions.
Damn Pirate, I hope you get this worked out well...I like you. Keep us informed of how this is going and what you are doing as well. Your in my thoughts dude.
I must not fear. Fear is the mind-killer. Fear is the little-death that brings total obliteration. I will face my fear. I will permit it to pass over me and through me. And when it has gone past I will turn the inner eye to see its path. Where the fear has gone there will be nothing. Only I will remain...
S'Ok Rocco, we'll get Pirate sorted out.
His problem isn't nearly as daunting as some cases that that I tackle.
TRuth be to datOriginally Posted by Trouble
Yeah, supplements often have bad dosing recommendations because they want it to seem like you are getting 60 days worth for x dollars when in fact it should be a 15 days supply.Originally Posted by Trouble
I appreciate everyone's support. I don't think I'm really in that bad of a position. I've likely got minor thyroid suppression, and I think the blood glucose thing will level out soon. I've got a strict and comprehensive diet and supplementation program in place now. I bet all bloodwork looks good after a month. I'm feeling optimistic.
Blood was drawn mid-afternoon, 100 minutes after eating a large burrito.
T3 uptake = 29.5%
T4 = 5.9 UG/dL
T7 = 1.74
TSH = 2.5
FSH = 1.4 MIU/mL
LH = 1.6 MIU/mL
TEST = 412 NG/dL
Others worthy of noting:
Glucose = 63 MG/dL
HEM A1C = 4.9%
HDL = 41 MG/dL
LDL = 50 MG/dL
Triglycerides = 126 MG/dL
Globulin = 1.8 G/dL
Albumin = 6.1 G/dL
A/G ratio = 2.4
GGT = 14 U/L
SGOT (AST) = 28 U/L
SGPT (ALT) 29 U/L
I’ll go back in for a fasting test for my lipids and glucose. The FSH, LH, and Test are all just about the same as they were a year ago, although my TSH has dropped a lot over the last few years (since my first cycle of gear).
The Globulin level bothers me more than anything. It is under the normal range, which makes my A/G ratio almost over the normal range. I’ve read that SHBG levels may be modestly reduced in hypothyroidism, acromegaly, Cushing's disease and hyperprolactenimia. Given that I just came off GH (acromegaly) and T4 (hypothyroidism), I'm inclinded to think my SHBG is in the shitter.
I’ll see my doc about getting more tests done. I’d like to know if there is a specific type of globulin that is real low. I’ve got more results, but these seem to be the only ones worth mentioning.
What do you think, Trouble?
You guys are toying with insulin control of the liver cholesterol cascade, and hence the trans-sulfuration and re-methylation pathways are dysregulated by unintended binding of steroid analogs to key nuclear receptors.
You are inducing hypogonadal insult and cardiovascular disease. Not correlated here, but also understood: changes in liver tryptophan metabolism, and the cascade of serotonin and dopamine down-regulation that is a key contributor to various neurochemical symptoms and disorders observed among chronic AAS users.
Know your tradeoffs.
Homocysteine induced cardiovascular events: a consequence of long term anabolic-androgenic steroid (AAS) abuse. Graham MR, Grace FM, Boobier W, Hullin D, Kicman A, Cowan D, Davies B, Baker JS. Br J Sports Med. 2006 Jul;40(7):644-8.
OBJECTIVES: The long term effects (>20 years) of anabolic-androgenic steroid (AAS) use on plasma concentrations of homocysteine (HCY), folate, testosterone, sex hormone binding globulin (SHBG), free androgen index, urea, creatinine, haematocrit (HCT), vitamin B12, and urinary testosterone/epitestosterone (T/E) ratio, were examined in a cohort of self-prescribing bodybuilders. METHODS: Subjects (n = 40) were divided into four distinct groups: (1) AAS users still using AAS (SU; n = 10); (2) AAS users abstinent from AAS administration for 3 months (SA; n = 10); (3) non-drug using bodybuilding controls (BC; n = 10); and (4) sedentary male controls (SC; n = 10). RESULTS: HCY levels were significantly higher in SU compared with BC and SC (p<0.01), and with SA (p<0.05).
--->Fat free mass was significantly higher in both groups of AAS users (p<0.01).
Daily energy intake (kJ) and daily protein intake (g/day) were significantly higher in SU and SA (p<0.05) compared with BC and SC, but were unlikely to be responsible for the observed HCY increases. HCT concentrations were significantly higher in the SU group (p<0.01). A significant linear inverse relationship was observed in the SU group between SHBG and HCY (r = -0.828, p<0.01), indicating a possible influence of the sex hormones in determining HCY levels. CONCLUSIONS: With mounting evidence linking AAS to adverse effects on some clotting factors, the significantly higher levels of HCY and HCT observed in the SU group suggest long term AAS users have increased risk of future thromboembolic events.
Steroids, sex hormone-binding globulin, homocysteine, selected hormones and markers of lipid and carbohydrate metabolism in patients with severe hypothyroidism and their changes following thyroid hormone supplementation. Bicikova M, Hampl R, Hill M, Stanicka S, Tallova J, Vondra K. Clin Chem Lab Med. (2003) 41(3):284-92.
Laboratory markers of thyroid function, selected steroid hormones, sex hormone-binding globulin (SHBG), homocysteine, prolactin, major markers of lipid- and glucose metabolism and of insular-growth hormone axes were investigated in fasting sera from 16 female patients with severe hypothyroidism after thyroidectomy because of thyroid cancer. The results obtained in severe hypothyroidism within 5-6 weeks after withdrawal of thyroid substitution therapy before control scintigraphy were compared with those obtained after correction of thyroid function. Elevated levels of homocysteine and prolactin in hypothyroidism significantly decreased after correction, while SHBG concentration increased.
--->Correction of thyroid function led to significant changes of growth hormone and immunoglobulin F1 (decrease and increase, respectively), while insulin and proinsulin increased only insignificantly. Elevated levels of total cholesterol and triglycerides in hypothyroidism were normalized, along with a significant increase in high density lipoprotein (HDL)-cholesterol.
--->As revealed by correlation and factor analyses, different relationships characterizing both states were found in hypothyroidism and after correction of thyroid function. A strong inverse relationship between homocysteine and free thyroid hormones confirms the effect of thyroid hormones on homocysteine metabolism. No such inverse relation was found in euthyroid state, however. Similarly, in hypothyroidism only, dehydroepiandrosterone sulfate correlated positively with immunoglobulin F1 and homocysteine and negatively with thyroid hormones and SHBG.
Just to make sure you get the message loud and clear:
Raised concentrations of C reactive protein in anabolic steroid using bodybuilders. Grace FM and Davies B. (same two labs as the first citation, clever Brits). Br J Sports Med. (2004) Feb;38(1):97-8.
OBJECTIVE: To examine levels of C reactive protein in users of anabolic androgenic steroids (AAS) compared with age matched control groups consisting of AAS using (but abstinent)/resistance trained and non-drug using/sedentary controls. METHOD: Subjects included AAS using bodybuilders (n = 10); bodybuilders who denied AAS use (n = 10); sedentary controls (n = 8). Venous blood was sampled, from which serum concentrations of C reactive protein, male sex hormones, and cardiac troponin T were determined. RESULTS: A significantly altered hormonal profile in the AAS using group provided indirect confirmation of AAS use. C reactive protein concentrations were significantly (p<0.05) higher in the AAS using bodybuilders. There was no relation between C reactive protein and cardiac troponin T.
CONCLUSION: AAS using bodybuilders had significantly higher C reactive protein concentrations, indicating a greater propensity to develop peripheral arterial disease.
(unfortunately, these Brits don't seem to understand the effect of androgen induced upregulation of LOX and COX pathway induced inflammation in erythrocytes. Remember, this also leads to red blood cell hyperplasia.
CRP and PAI expression are upregulated by sterol nuclear receptor protein SRC-1; I have laid out a nice, albeit technically dense, explanation on M2 (Mind and Muscle forums), in several threads on X-Factor/arachidonate metabolism and the nuclear receptors activated by its presence.
Sex steroids alter AA expression, via several routes, all of whose buttons are pushed by supraphysiological doses of steroid analogs.
Effect of homocysteine on arachidonic acid release in human platelets.
Signorello MG, Pascale R, Leoncini G. Eur J Clin Invest. (2002) 32(4):279-84.
BACKGROUND: It has been suggested that homocysteine is implicated in the risk of atherosclerosis and thrombosis. The pathogenic mechanism has not been clarified, but oxygen-free species produced by the homocysteine metabolism and auto-oxidation could have a role. DESIGN: We have studied the effect of homocysteine on arachidonic acid release in human platelets. Two important products of arachidonic acid metabolism - thromboxane B2 (TXB2) and reactive oxygen species (ROS) - have been assayed.
RESULTS: Results indicate that homocysteine induces arachidonic acid release that is partially inhibited by 5,8,11,14-eicosatetraynoic acid (ETYA). Platelet incubation with homocysteine significantly increases basal levels of TXB2 and ROS. The effect is time- and dose-dependent. The TXB2 formation is strictly correlated with the arachidonic acid release. Moreover, ROS accumulation is largely inhibited by ETYA and partially reduced by diphenyleneiodonium (DPI), suggesting the involvement both of enzymes metabolising arachidonic acid (cyclooxygenase (COX), lipooxygenase (LOX), and cytochrome P450 monooxygenase) and of NAD(P)H oxidase).
(technical insert by moderator- note that hyperglycemia induced glycation, a primary cardiovascular alteration process, is carried out by iron (not heme, free iron) catalyzed free radical promotion by NADPH attack on glucose. Secondary fuckup, fibrinogen is attacked by ROS produced by AA, and that leads to "remodeling" of the vascular system = becomes stiffened and unable to relax, inducing *permanent* blood pressure changes. If you do a PubMed search on homocysteine and AAS, you will pull up fairly recent citations that verify this cascade. This explanation is provided specifically for dg and to provide further connections between AAS use and side effects reported from its chronic use.
Ask the logical question: why is iron elevated? Because its part of a chain reaction cascade, previous cellular damage to red blood cells attacks at heme centers in hemoglobin proteins, and this releases iron from its porphorin complex, as free iron. Back to the cited abstract....
CONCLUSION: Homocysteine induces oxidative stress in human platelets in vitro. The unbalance in platelet redox-state and the increased TXB2 formation may generate hyperactivation, contributing to a thrombogenic state leading to cardiovascular diseases.
god, the beauty of these biochemical connections is staggering.
Last edited by Trouble; 08-02-2006 at 11:26 AM.