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I am come across some of the most complicated cases that are out there and I would like to share of one them.
The patient was a 43 year old male that was on TRT at 200 mgs a week when he first came into the office. He had 3 rhein urine test done and all of them where taken on the 4 th day of the injection as well as the blood. The patient testosterone was testing at 1400 which was extremely high, but the 24 hour was testing deficient not just one test all 3 urine labs.
He was on adex at 1.5 mgs a week and e2 was in check in the blood test at 30, shbg 15. I know that there are hyper excretors, but this is the first scenerio of where I saw i hypo case.
We examined all other hormone and the patient has very strong adrenals, but had had TSH but low levels of total thyroid hormones. He also tested deficient in selenium and zinc which could explain his high rt3.
Now in my research I have found articles that dealt with zinc deficiency that could affect androgen receptor down regulation by significant amount. Another article also pointed out that selenium was also potentially responsible for testosterone receptor sensitivity as well. Now would one start to look at potential testosterone antibodies (if they exist) or potential rare case of androgen resistance.
Could fixing the thyroid push the testosterone into the tissue like cortisol does with thyroid to increase ultization?
I suggested 400 mcg of selenium and 50 mgs of zinc picolonate for 8 weeks then retest to see if there was any changes.
This is one case that every one stumped, but so far I have begun to make some lee way getting his well being back to some what normal.
By lowering the testosterone down to 140 mgs a week he did feel better, but his numbers where actually lower in the urine. One can not always go by clinical testing all the time. I have an idea that this person may be a super rare case of what is known as paradoxical as I have came across one other case similar. Thought this would be interesting to share.
@hardasnails1973 277 wrote:
The patient was a 43 year old male that was on TRT at 200 mgs a week when he first came into the office. He had 3 rhein urine test done and all of them where taken on the 4 th day of the injection as well as the blood. The patient testosterone was testing at 1400 which was extremely high, but the 24 hour was testing deficient not just one test all 3 urine labs.
He was on adex at 1.5 mgs a week and e2 was in check in the blood test at 30, shbg 15. I know that there are hyper excretors, but this is the first scenerio of where I saw i hypo case.
We examined all other hormone and the patient has very strong adrenals, but had had TSH but low levels of total thyroid hormones. He also tested deficient in selenium and zinc which could explain his high rt3.
Now in my research I have found articles that dealt with zinc deficiency that could affect androgen receptor down regulation by significant amount. Another article also pointed out that selenium was also potentially responsible for testosterone receptor sensitivity as well. Now would one start to look at potential testosterone antibodies (if they exist) or potential rare case of androgen resistance.
Could fixing the thyroid push the testosterone into the tissue like cortisol does with thyroid to increase ultization?
I suggested 400 mcg of selenium and 50 mgs of zinc picolonate for 8 weeks then retest to see if there was any changes.
This is one case that every one stumped, but so far I have begun to make some lee way getting his well being back to some what normal.
By lowering the testosterone down to 140 mgs a week he did feel better, but his numbers where actually lower in the urine. One can not always go by clinical testing all the time. I have an idea that this person may be a super rare case of what is known as paradoxical as I have came across one other case similar. Thought this would be interesting to share.
There is much that is not clear to me.
* For example, for what reason did the patient come for help?
* Was if for depression, lack of energy, lack of libido, impaired concentration and memory, etc.?
* Why is this patient so unusual or complicated?The nuclear receptors of certain hormones, such as testosterone, have zinc as a component (the zinc fingers noted in texbooks). Zinc deficiency may impair receptor production.
Four days after a single testosterone cypionate injection of 200 mg, the testosterone level should be around 650 ng/dl if the half-life of testosterone cypionate is the usual 7 days. When the 4-day level is very high, then the half-life of testosterone cypionate is very long. The dosage of testosterone cypionate then needs to be lowered so that testosterone may be in a physiologic range.
* In what way was the patient deficient in testosterone on urine testing, when he had a blood level of 1400?
* Were the testosterone metabolites deficient?* Total thyroid hormone is “low”. But how low?
* And what was the TSH?* Why was Arimidex used?
* Did function improve when estradiol was reduced?
* Were there clear signs of estrogen excess?Reducing estradiol excessively may reduce the number of testosterone receptors.
Testosterone is lipid soluble. It gets into cells easily by diffusion. Whether or not it triggers actions in the cell depends on whether or not it has a receptor to bind to.
If actual thyroid hormone levels are low, a person is going to have problems with hypothyroidism, even if TSH is “normal” or even “low”.
TSH is not a good measure of thyroid hormone if metabolic issues are in play. TSH assumes the nervous system is working well. But if the nervous system is not working well, then TSH can be low or normal while actual thyroid hormone levels are low.
The testes produce not only testosterone, but thyroid releasing hormone. Exogenous Testosterone replacement therapy can lower thyroid hormone production, leading to problems, as testicular testosterone releasing hormone is reduced.
* Why does this case stump you?
I’m interested to know the answer to this and the above questions.
The patient was exhibiting low libido, slight depression, excessive weight gain around stomach, in ability to put on muscle mass, fatigue, mental fog When he first came to us he was one grumpy old man at 43 is the most clinical diagnosis.
He had been on 200 mgs of test from anti aging clinic with .5 mwf adex felt great for about 5 months then all of sudden family started getting on him about how TRT goes against nature. He pressured by family and he stopped TRT abruptly and felt horrible. Went to a Dr and was prescribe hcg which his T barely went up, but e2 was 63. The patient tried adex, but was at almost 3 mgs a week numbers did not change.
The rheins urine testosterone metabolites were all out of range low on hcg and later on 200 mgs of testosterone. When he was taking 200 mgs of testosterone he was measuring 1400(300-1100) at day 4 on the draw and e2 of 22 from ultrasensitive with shbg of 18, dht 60. At this time he was taking 1 mgs of adex EOD. When the urine metabolites where taken of the 4 day of shot testosterone metabolites where all low normal and e2 , dht urine metabolites were high in relationship to testosterone metabolites. Every thing look GREAT in the blood (may be T was high, but e2 (22) and shbg (20) was in check), but urine reflected more of the true clinical picture.
After reducing his testosterone down to 160 mgs (80mgs BIW) and reducing adex down to .5 EOD after 8 weeks his symptoms vastly improved. At his next visit his wife came in and commented on how much his mood has changed and was so emotional she even started to cry. The patient symptoms of depression and stable mood got noticeably better. He was smiling and joking around. One would swear it was not the same person.
We ran an EFA fatty acid test which should alot of imbalances.
The 2 things that were done to get the best results were correcting his fatty acid imbalances and adjusting TRT.
His TSH was 3.5. Since we didn’t understand the thyroid as much as we do now further thyroid test resulted in mid range total 4 and low normal t-3 (105 97-220) and elevated rt3 (35 11-32) which we over looked first time His previous thyroid readings were normal mid range of ft4, ft3.
Since reading your post on thyroid testing it enable us to correct the errors that were made in over 40 thyroid cases that had to be re evaluated.
Since he was identified as having a selenium and zinc deficiency we decided to supplement with the proper nutrients and retest in 6 weeks to see if there was a clincal response.
We did not intiate thyroid medicine at this time, but may if the thyroid parameters have not changed.
Last time we spoke he was doing better then he has been in few years and has a positive out look on issues vs the gloomy and doom person I met a year ago.
One interesting not is that he feels better when he went on vacation in germany. I found out the reason why is because he would goto the spa to detox in sauna and pools for several hours. This could be a huge part of the puzzle as he used to paint cars when he was younger all the time with out proper protections. He also worked in priniting press with being exposed to silk screen vapors and other dangerous vapors. When he gets the room in his house he plans on getting an infrared sauna which should be a great asset to improving his well being. Detoxification was one of the biggest contributers to increasing his well being along with proper hormone manipulation.
The initial blood levels of testosterone and estradiol were not that great. Testosterone to estradiol ratio was too high. Testosterone was too high. Remember, that I prefer a 20:1 to 30:1 testosterone to estradiol ratio. The levels you showed were 44:1.
The urine test showed testosterone was being metabolized a lot to DHT and estradiol – both of which are being actively used in signaling. This would be expected with a high testosterone level. Arimidex may prevent the production of estradiol. However, there are other pathways to create estrogens that testosterone can go through. John Crisler, MD noted that often on Arimidex, the other estrogen metabolites would test high. This would be a more prominent problem with supraphysiologic testosterone levels. Testosterone has to be metabolized toward something. Arimidex just blocks the estradiol/estrone pathways but not the others. Reducing testosterone dose helps reduce pressure to go through these other pathways, as well as reducing the Arimidex dose.
In some ways, forcing testosterone to metabolize through alternative estrogen pathways and excessive DHT is not that useful. Some estrogen metabolites can cause DNA damage and excessive oxidative stress. This is where perhaps keeping testosterone within a physiologic range (the day 2 peak of a 200 mg injection should be 1200), and using a limited amount of Arimidex may be more useful.
Dihydrotestosterone (DHT) at high levels can also cause insulin resistance. This would impair energy production, nervous system function, etc.
The average American TSH of 3.5 is too high. Improvement in mood can sometimes occur despite the presence of hypothyroidism. This occurs when the stress/norepinephrine signaling is not too high, and can actually work to help generate energy, e.g. by improving production of deiodinases, and adrenal function is intact and capable of adapting to a high stress state. But the continued presence of hypothyroidism and compensatory elevated sympathetic nervous system activity is not a stable long-term condition. Sooner or later, hypothalamic-pituitary-adrenal dysregulation can occur, setting the stage for adrenal fatigue and deterioration in the person’s condition. Sometimes a patient is satisfied being in this state and would not want a change. AFter discussion about the pitfalls, I would continue the present compromised position and monitor it going forward, ready to adjust thyroid should the need turn up.
@DrMariano 306 wrote:
The initial blood levels of testosterone and estradiol were not that great. Testosterone to estradiol ratio was too high. Testosterone was too high. Remember, that I prefer a 20:1 to 30:1 testosterone to estradiol ratio. The levels you showed were 44:1.
The urine test showed testosterone was being metabolized a lot to DHT and estradiol – both of which are being actively used in signaling. This would be expected with a high testosterone level. Arimidex may prevent the production of estradiol. However, there are other pathways to create estrogens that testosterone can go through. John Crisler, MD noted that often on Arimidex, the other estrogen metabolites would test high. This would be a more prominent problem with supraphysiologic testosterone levels. Testosterone has to be metabolized toward something. Arimidex just blocks the estradiol/estrone pathways but not the others. Reducing testosterone dose helps reduce pressure to go through these other pathways, as well as reducing the Arimidex dose.
In some ways, forcing testosterone to metabolize through alternative estrogen pathways and excessive DHT is not that useful. Some estrogen metabolites can cause DNA damage and excessive oxidative stress. This is where perhaps keeping testosterone within a physiologic range (the day 2 peak of a 200 mg injection should be 1200), and using a limited amount of Arimidex may be more useful.
Dihydrotestosterone (DHT) at high levels can also cause insulin resistance. This would impair energy production, nervous system function, etc.
The average American TSH of 3.5 is too high. Improvement in mood can sometimes occur despite the presence of hypothyroidism. This occurs when the stress/norepinephrine signaling is not too high, and can actually work to help generate energy, e.g. by improving production of deiodinases, and adrenal function is intact and capable of adapting to a high stress state. But the continued presence of hypothyroidism and compensatory elevated sympathetic nervous system activity is not a stable long-term condition. Sooner or later, hypothalamic-pituitary-adrenal dysregulation can occur, setting the stage for adrenal fatigue and deterioration in the person’s condition. Sometimes a patient is satisfied being in this state and would not want a change. AFter discussion about the pitfalls, I would continue the present compromised position and monitor it going forward, ready to adjust thyroid should the need turn up.
Dr M,
Thank you for that detailed explanation. My plan was to watch to see how the nutrient intervention is going to affect thyroid function. If there is little or no change then thyroid supplementation is going to be implemented at low dosages. With every client their adrenals are monitored before and 8 weeks into thyroid treatment by saliva cortisol test. Some times we have found people with strong adrenals (you mention above) get caught in a comfort zone for a long time. When a person who is given armour thyroid medication one can see even the strongest adrenals end up becoming fatigue in a short amount of time. Giving the patient thyroid it could uncover a hidden cortisol imbalance. By challenging the function of the adrenals by adding more thyroid one would see if they are able to handle the extra stress of the thyroid. In one instance a patient with high cortisol level with low t4 and t-3 total numbers when given thyroid caused the cortisol levels to normalize. The clinical response was improved libido, mood, and energy levels issued that unresolved by proper TRT.
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