Thyroid Labs for Dixiewrecked

DixieWrecked

Well-Known Member
I have been taking 1.5 grain of compounded NDT for about a month along with Selenium and a trace mineral supplement. Here are my current numbers.
________________________________________________________________________________________________________________

TSH: not included, thought it was

Free T3: 3.5
T3 Range: 2-4.4

Reverse T3: 25.3 high
Reverse T3 range: 9.2-24.1

Free T4: 1.36
T4 Range: 0.82-1.77

TPO and antibodies were totally healthy undetectable
________________________________________________________________________________________________________________

I essentially don't feel any different than before. The reason I started taking NDT is becuase it was originally prescribed by Defy about 6 years ago but I never went down that path. I finally thought I would try to address this because I feel like my energy is suboptimal. The reason they prescribed NDT 6 years ago was to treat a TSH of 2.7. Is the best course of action to switch to a lower dose of NDT and add in some T3?

Thanks for taking the time to read.
 
I'm not saying this applies to you, but I went down the thyroid rabbit hole with Defy and now think it's a case of treating the side effects without looking into the underlying cause. I had top-of-range reverse T3, which they treated with a T3 prescription. It brought down rT3, but didn't seem to do much else. As I migrated to lower TRT doses I dropped the T3 and rT3 was normal. Grok says it's plausible that excessive testosterone can in some cases raise rT3.

Yes, it is plausible that an excessive dose of testosterone could raise reverse T3 (rT3) levels, particularly in the context of high-dose anabolic androgenic steroid (AAS) use or supraphysiological testosterone replacement therapy (TRT), based on studies showing mild thyroid impairment and patterns resembling low T3 syndrome (also known as non-thyroidal illness syndrome or euthyroid sick syndrome), where rT3 is often elevated.Evidence for Plausibility
  • Studies on AAS (which include testosterone derivatives like nandrolone decanoate) in animal models and humans demonstrate alterations in thyroid function that could favor rT3 elevation. For example, chronic AAS administration in rats led to decreased serum total T3, free T4, and TSH, with increased type 1 deiodinase (D1) activity in the liver and kidney. D1 converts T4 to both T3 and rT3, but in states of thyroid impairment, the balance can shift toward rT3 production.
  • In human bodybuilders self-administering high-dose AAS, there were significant decreases in total T3 and T4, reduced thyroxine-binding globulin (TBG), and a blunted T3 response to thyrotropin-releasing hormone (TRH), indicating relative thyroid dysfunction within the normal range. This low T3 pattern mirrors non-thyroidal illness syndrome, where rT3 is typically elevated as part of an adaptive response to stress or metabolic changes, though rT3 was not directly measured in these studies.
  • Anecdotal reports from TRT users suggest elevated rT3 in some cases, alongside symptoms of hypothyroidism (e.g., fatigue, low libido), with lab changes like increased TSH and decreased T3 after prolonged high-dose use. However, this is not universal and may depend on individual factors like dose, duration, and concurrent dieting or training stress.
  • In contrast, physiological elevations in testosterone (e.g., in PCOS, where women have naturally higher testosterone) do not show elevated rT3; instead, free T3 and T4 are often higher, suggesting the effect is dose-dependent and more pronounced at supraphysiological levels.
 
Cat, thanks for that bad ass reply and sharing your experience and quick research.

I also have a saliva cortisol test that was sent in, and I am awaiting the results. My initial layman's thought is that high doses of test affect adrenal function and alter cortisol production and this in turn raises RT3. There are several new age thyroid gurus that state that cortisol affects RT3.

At any rate, the need for polypharmacy to sustain higher dose androgens seems really challenging.
 
Cat, thanks for that bad ass reply and sharing your experience and quick research.

I also have a saliva cortisol test that was sent in, and I am awaiting the results. My initial layman's thought is that high doses of test affect adrenal function and alter cortisol production and this in turn raises RT3. There are several new age thyroid gurus that state that cortisol affects RT3.

At any rate, the need for polypharmacy to sustain higher dose androgens seems really challenging.
Treating the thyroid can be a tough process. Most people I know feel no different. I do use thyroid meds to help lower my LDL particle numbers.

I use 90 mg of thyroid armor in the morning and 6.25MCG of t3 morning and afternoon.
 
So the plot thickens. Looks like my cortisol is kind of messed up. I have attached the labs. Apparently low cortisol can increase RT3 so I am going to attempt to mitigate this with licorice root extract and panax ginseng. Morning and noon cortisol levels were middle of the range and have room to increase for sure. But this low cortisol after lunch is most likely why I am only on the ball for half a day at most. My dhea went from almost 400 to 200 since starting TRT which, along with this data proves to me that TRT has dramatically reduced my adrenal function.

I'll keep this threaded updated in case anyone is interested.
 

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My 2 cents, I agree that sounds low. Are you taking any glucocorticoids like Hydrocortisone, Prednisone, Triamcinolone? Azole antifungals? Opiates?

I'd test cortisol at 8am along with ACTH. Anything under 10 ug/dl at 8am, especially with low or low normal DHEAS, then I'd pursue adrenal stimulation testing. Especially if you have any of the following:
"Patients with adrenal insufficiency typically present with nonspecific symptoms, including fatigue (50%-95%), nausea and vomiting (20%-62%), and anorexia and weight loss (43%-73%)."

 
This is from OpenEvidence:
Glucocorticoids—including oral, intravenous, inhaled, topical, intra-articular, and intranasal formulations—are the medications most commonly associated with disruption of the normal daily cortisol rhythm. Chronic or supraphysiologic dosing suppresses the hypothalamic-pituitary-adrenal (HPA) axis, leading to a blunted or flattened diurnal cortisol profile, loss of the early morning peak, and low late-night nadir. Long-acting agents such as dexamethasone and betamethasone are particularly potent in suppressing circadian cortisol secretion, while intermediate- and short-acting agents (prednisone, prednisolone, hydrocortisone) also disrupt the rhythm if administered inappropriately, especially at night. The Endocrine Society and the European Society of Endocrinology jointly emphasize that any route and dose above physiologic replacement can suppress the HPA axis and alter cortisol rhythmicity.[1]
Opioids (e.g., morphine, oxycodone, fentanyl) can also suppress CRH and ACTH secretion, leading to secondary adrenal insufficiency and disruption of the normal cortisol rhythm, though the degree of suppression varies by agent and individual.[2]
CYP3A4 inhibitors (e.g., ritonavir, ketoconazole, clarithromycin, grapefruit juice) can increase circulating glucocorticoid levels when co-administered, thereby enhancing HPA axis suppression and further flattening the cortisol rhythm.[1][3]
Psychotropic medications—notably antidepressants and antipsychotics—are associated with reductions in basal and stimulated cortisol levels, and may blunt the cortisol awakening response, although effects are variable and less pronounced than with glucocorticoids.[4]
In summary, the most clinically significant disruption of the normal daily cortisol rhythm is caused by exogenous glucocorticoids, with additional contributions from opioids, CYP3A4 inhibitors, and certain psychotropic agents.[1-4]
 
My 2 cents, I agree that sounds low. Are you taking any glucocorticoids like Hydrocortisone, Prednisone, Triamcinolone? Azole antifungals? Opiates?

I'd test cortisol at 8am along with ACTH. Anything under 10 ug/dl at 8am, especially with low or low normal DHEAS, then I'd pursue adrenal stimulation testing. Especially if you have any of the following:
"Patients with adrenal insufficiency typically present with nonspecific symptoms, including fatigue (50%-95%), nausea and vomiting (20%-62%), and anorexia and weight loss (43%-73%)."

Man thank you so much for sharing all this knowledge.

Currently I use kratom. Not an insane amount but it gets me going despite the lethargy ive experience for years. Maybe that causes some disruption similar to opioids.

I also started 10mg of Lexapro about 3 months ago. Again well after this lethargy problem.

My 8am cortisol test was only at a 10. Noon was around 10 as well. So it seems in general I kind of follow the correct curve but it's just low.

This old nutrition guru and owner of the vitamin store near me, who is like an encyclopedia, says that panax ginseng can get things going again. Increase stimulation of the entire adrenal system. I'll have to research that more.
 

Here is a thread of me feeling the exact same way 3 years ago. Pretty much the same thyroid numbers. But I wasn't taking any kratom or Lexapro.
 
My 8am cortisol test was only at a 10. Noon was around 10 as well. So it seems in general I kind of follow the correct curve but it's just low.
Am I understanding this correctly? 8am cortisol was 10 ug/dl, then at noon it was still 10 ug/dl?
What time do you normally wake up? If you normally wake up around 4am then it may be normal.

Noon cortisol should be somewhere around 1/2 the morning cortisol level. A flat cortisol curve can be associated with ME/CFS myalgic encephalomyelitis/chronic fatigue syndrome.

In which case it might be helpful to read through this and see if that fits:

Testing and treatment recs from ME/CFS Clinician Coalition:
 
I also started 10mg of Lexapro about 3 months ago. Again well after this lethargy problem.
Lexapro can possibly effect cortisol testing. Am I correct in guessing that it hasn't helped with the lethargy?

OpenEvidence:
Escitalopram can affect cortisol blood tests. Multiple randomized controlled trials and clinical studies have demonstrated that escitalopram, a selective serotonin reuptake inhibitor (SSRI), modulates hypothalamic-pituitary-adrenal (HPA) axis activity and alters cortisol secretion in both healthy individuals and patients with psychiatric disorders.

Acute administration of escitalopram has been shown to transiently increase plasma and salivary cortisol levels in healthy volunteers, reflecting central serotonergic activation.[1-2] However, with longer-term administration (weeks to months), escitalopram tends to decrease baseline cortisol levels and normalize HPA axis hyperactivity, particularly in populations with elevated baseline cortisol such as patients with depression, panic disorder, or generalized anxiety disorder.[3-6] For example, in older adults with generalized anxiety disorder, 12 weeks of escitalopram treatment led to significant reductions in both peak and total salivary cortisol compared to placebo.[6] Similarly, in patients with panic disorder, 12 weeks of escitalopram reduced both ACTH and cortisol levels.[4]

The effect of escitalopram on cortisol is dose-dependent and time-dependent. Short-term use may increase cortisol acutely, while chronic use is associated with normalization or reduction of elevated cortisol, especially in those with HPA axis dysregulation.[3][5-6] These changes can be detected in both plasma and salivary cortisol assays.

Therefore, when interpreting cortisol blood tests in patients taking escitalopram, it is important to consider the timing and duration of SSRI therapy, as it can confound assessment of HPA axis function and cortisol-related diagnostics.[3][5-6]
 
Was your reverse T3 similarly high before you started supplementing NDT? I don't see your baseline thyroid labs here. Are we sure rT3 isn't high as a result of the intervention?
I think the NDT is probably raising my RT3. I don't have a baseline because defy prescribed upon my initial consultation based on a tsh around 2.8. so I'm not sure about RT3 with no thyroid meds.
 
Am I understanding this correctly? 8am cortisol was 10 ug/dl, then at noon it was still 10 ug/dl?
What time do you normally wake up? If you normally wake up around 4am then it may be normal.

Noon cortisol should be somewhere around 1/2 the morning cortisol level. A flat cortisol curve can be associated with ME/CFS myalgic encephalomyelitis/chronic fatigue syndrome.

In which case it might be helpful to read through this and see if that fits:

Testing and treatment recs from ME/CFS Clinician Coalition:
8 am was 10. Noon was 10. 4pm was 2.9. 8pm was 3.1.

I'll check out those threads when I get back to my place. Thanks again for the help
 
I think the NDT is probably raising my RT3. I don't have a baseline because defy prescribed upon my initial consultation based on a tsh around 2.8. so I'm not sure about RT3 with no thyroid meds.
A TSH of 2.8 without the rest of the thyroid labs doesn't support supplementing thyroid hormone. That would be like starting TRT because your LH was on the high side of normal.

Similarly to hypogonadism, many symptoms of hypothyroidism are non-specific and shared by many other causes. In these "subclinical" cases, from what I've seen, supplementing thyroid hormone rarely helps.

IMO, in the absence of clear pathology, the body is very intelligent in its regulation of thyroid hormone and metabolism and it should not be tampered with. If you are in a caloric deficit, if you're eating low carb, etc, the body tunes the thyroid axis appropriately in response. Our manually supplemented hormones are very crude in comparison.

I'd like to see your full thyroid labs when you are off NDT and eating at maintenance calories. I bet there's nothing wrong there.
 

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