What are the clinical triggers—among them, lack of symptom control, inability to achieve normalization of thyroid hormone function biomarkers/tests, treatment failure with T4, and metabolic co-morbidities affecting T4-to-T3 conversion—that prompt you to consider a person an ideal candidate for DTE-based hormone replacement?
So when we are assessing thyroid levels, we are looking at numbers, obviously. We're looking at the TSH, the free T4, the free T3, and in my case, the reverse T3. I am trying to ensure that the thyroid levels aren't just in the reference range. And the reference range, as we well know, is derived from a reference population. Um, I really do try to optimize the levels, meaning that I want the TSH between about 0.5 to 2, 2.5. That is what the Enhanes study ultimately decided was a normal TSH and what some of the organizations have come out afterwards to say is a normal TSH. I don't want it to be 4 and 5, which is still in the reference range. For free T4 and free T3, I like that middle category, you know, the median of the reference range, um, and reverse T3, again, the median of the reference range, as good as I can get. Sometimes it's not perfect, um, but we're really trying to optimize levels, not just get it into a reference range. If we've done that and the patient is still symptomatic, if they still have hypothyroid symptoms. Then we would consider maybe switching formulations. Usually though, in my clinical practice, if we've optimized all of those levels and they're still having symptoms consistent with hypothyroidism, it's usually a different issue. So these patients have comorbidities that can look very similar to hypothyroidism, iron deficiency, very common micronutrient deficiency that we see, especially in young women who are menstruating. Um, we see sleep apnea, we see, um, hypoglycemia, we see other, um, micronutrient deficiencies and, um, perimenopause, other medical issues that may be contributing to very similar symptoms that the patient might be attributing to hypothyroidism, depression, anxiety. Um, and typically, if we go down that path, we can optimize symptoms by addressing all of those different things. Now, if I had somebody on LT4 monotherapy and they, you know, we had addressed everything and we looked at everything, um, numbers wise and we think we're good, um, with the numbers, then we could try combination therapy in those patients. Um, and then the question is, well, what do you do? Do you go on. Um, T4 plus T3, you know, dual therapy, human bioidentical, or do you jump straight to DTE products, desiccated thyroid extract, and how do you determine what? In my practice, I can use both equally, honestly, but Um, the differences are these. Number one, if you do T4-T3 combination therapy, you need to know how to dose them correctly. In my practice, when I'm adding liothyronine, I usually dose it twice a day, um, at minimum because it doesn't last for the full 24 hours. And I've also found that liothyronine is very, very instant release. So in patients who are very sensitive to T3 products, They tend to do much better on the DTE products, and that probably is because of the fact that DTE has thyroglobulin within it and other fillers within the tablet that may make it a little gentler when absorbed. Liothyronine or Cytomel is super instant release. It will peak within an hour or two of taking the medication. And patients who are either sensitive or in my postmenopausal females who don't have the same capacity to bind to thyroid hormone because they don't have female hormones around. They don't have the lack of female hormones. Drops their TBG binding protein, which preferentially binds to T4, but can also have some binding affinity to T3, or they're malnourished or they have sarcopenia and they just can't tolerate such a high peaking of T3, they may do better with the DTE products. Also, if you're going to try for T4 and T3 combination therapy, you as a provider need to know how to interpret the labs and how to dose and titrate the medication correctly. Um, so whether you start at baby dosing of T3, sometimes they start with 2.5 mcg, or if you're having to use higher doses, you really need to know how to titrate them individually versus DTE products which come at a ratio of 4:1, T4 to T3. The normal physiology of thyroid hormone from the thyroid is 14 to 1 with regard to T4 and T3, um, and then you're basically taking that T4 and you're making a set amount of T3 every day. Um, say you have somebody who has that DIONase function, that conversion function completely shut off. Maybe they have obesity, um, where they don't really have muscle mass to convert well. And by the way, fat mass or adipose tissue has DIONase 3 in it, and that's an inactivating enzyme, so reverse T3 will go up. Um, so that That can be a reason. They could have a genetic reason for not converting T4 to T3 well. They could be on steroids lifelong, say they have asthma, or if they have really bad osteoarthritis and a lot of inflammation, they're not going to convert T4 to T3. If you know that going in, you know that that conversion process is pretty much going to be at 0%. And if that's the case, going to a DTE product 4 to 1 is basically replacing both T4 and T3 without relying on the conversion, the natural conversion that should happen in a patient who doesn't have inflammation going on and can work with a 14:1 ratio. Um, so both options will work, but if you're doing T4, T3, um, individually, you just as a provider need to know that there's going to be titration involved. If you have a patient off the off the bat that is sensitive to T3 medication or that has complete shutdown of that T4 to T3 conversion process, then a DTE product may be the way to go.
