In search of Endocrinologist or thought leader concerning complex thyroid conditions.

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Hello,

There are many people here, including myself, with complicated thyroid issues. My goal is to find an endocrinologist or thought leader in the area of thyroid treatment. I noticed that the author of the book "Stop The Thyroid Madness" (Janie A. Bowthorpe, M.Ed) offers one-on-one consultation. Do you know of anyone that has participated in a call with her and had success?
 
Defy Medical TRT clinic doctor
Id trust a handful of the membership on this forum to delve in your Thyroid and that's free. We have some great knowledge represented in that area.
 
Thank you very much,

This maybe too much information but wanted to provide a background. 59-year-old male. Patient at Defy since 12-1-2018. Prescribed 50mcg liothyronine qd for the past 40 days. No changes in my weight. I have had a life-long struggle with weight (fat) loss. At 5’ 10” my goal is to weight 200 pounds. I have lifted weights and done cardio exercise for the past 35 years. This 30-day example is representative to how I have been eating and exercising for the past 20+ years. During this 30-day example I was alcohol free, included weight training, and cardiovascular workout (elliptical). Starting weight 242, ending weight 240 with a 30-day caloric deficit of 51,667. I understand body weight may vary with fat vs muscle and included results of dexa below. However, they are not with the 30-day period of this sampling.



Dexa total body Total Mass Fat Tissue Lean tissue BMC Visceral fat

Fat% lbs. lbs. lbs. lbs. lbs.

3-11-19 28.9% 241.8 69.9 162.9 8.9 4.58

1-4-19 30.9 242.3 74.9 158.4 9.0 5.29



3-1-18 resting metabolism rate.

Weight 238

RMR = 2183

Predicted RMR = 1892

Deviation 115%

Metabolic Speed = fast





Example of 30-day tracking, 2-11-19 to 3-11-19



Week Protein Fat Carbs

1 892 380 1002

2 638 236 725

3 1099 312 1114

4 1177 346 1196



Week caloric Calories Caloric

intake burned deficit

1 11102 24032 12930

2 10358 21390 11032

3 14001 28081 14080

4 12972 26597 13625







12-1-18

Range

Reverse T3 20.3 ng/dl 9.2-24.1

T3, free 3.2 pg/ml 2.0-4.4

Thyroxine (T4) Free 1.24 ng/dl 48-344

TSH 2.040 uIU/ml 0.450-4.500

Luteinizing 0.1 mIU/mL 1.7-8.6

Hormone

Thyroglobulin (<1) IU/mL 0.0-0.9

antibodies

Thyroid peroxidase 9 IU/mL 0-34

(TPO) antibodies



3-18-19

Reverse T3 19.3 ng/dl 9.2-24.1

T3, free 3.6 pg/ml 2.0-4.4

Thyroxine (T4) Free 1.06 ng/dl 48-344

TSH 2.630 uIU/ml 0.450-4.500



Not included in the 3-18-19 lab results

Luteinizing 1.7-8.6

Hormone

Thyroglobulin 0.0-0.9

antibodies

Thyroid peroxidase 0-34

(TPO) antibodies



 

Cataceous

Super Moderator
Thanks for the quick reply! I am currently taking 50 mcg of liothyrinine. Would you say this dose needs to increase until the T3 levels are <15?
Are you sure about that dose of liothyronine? My rT3 was even higher and Defy has me on a trial titrating upwards from 5 mcg qd. In any case, my understanding is that you haven't had new lab work since starting the medication. So that will be important, along with a subjective evaluation.
 

Vince

Super Moderator
I would have to agree that is a pretty high dose of synthetic T3. I'm surprised it hasn't moved down your reverse T3 more. Do you take your thyroid meds in the morning a 1/2 hour before you eat anything, drink anything besides water or black coffee.
 
I would have to agree that is a pretty high dose of synthetic T3. I'm surprised it hasn't moved down your reverse T3 more. Do you take your thyroid meds in the morning a 1/2 hour before you eat anything, drink anything besides water or black coffee.
Yes, I get up take my T3 with a glass of water and wait and hour before food or coffee. Just switched from the compounded pharmacy T3 to branded synthroid. Not sure if there is a big difference but some swear by branded. Any thoughts on that topic would be appreciated.
 

Vince

Super Moderator
Yes, I get up take my T3 with a glass of water and wait and hour before food or coffee. Just switched from the compounded pharmacy T3 to branded synthroid. Not sure if there is a big difference but some swear by branded. Any thoughts on that topic would be appreciated.
Levothyroxine (synthroid) is a synthetic version of T4, and liothyronine (Cytomel) is a synthetic version of T3.
 
Are you sure about that dose of liothyronine? My rT3 was even higher and Defy has me on a trial titrating upwards from 5 mcg qd. In any case, my understanding is that you haven't had new lab work since starting the medication. So that will be important, along with a subjective evaluation.
I am going to call monday to schedule a lab and a consultation. We started at 10mcg, titrated to 20 mcg and I waited 3 months for my next lab, then they had me titrated to 50 mcg. I want a more aggressive titration schedule and plan of action. Thanks.
 
This is the problem, your reverse T3 should be <15, indicates that the T3 that you do have is pooling and not making it in to your cells.

Typical treatment is to add T3 daily. Your T4 levels are typical and not unusual.

Hi Vince,

I really appreciate you help. When you have an opportunity would you please let me know where or how you learned that the value of reverse T3 should be below 15? I would like to be more educated about my lab values and how they should be treated. Since this post I read 2 books, "Stop the Thryroid Madness II and Recovering wit T-3. Both are interesting reads but do not cover this topic.

Thanks,
 

Cataceous

Super Moderator
If you're interested in an opposing view on the importance of reverse T3 results, here's a skeptical blog from ZRT: Reverse T3 – Why It’s Not Useful for Routine Thyroid Testing

... Since high rT3 is linked with conditions associated with slow metabolism, it has been claimed in internet articles, but not in peer-reviewed papers, that rT3 causes a slowing in metabolism by blocking or obstructing the nuclear thyroid receptors. These receptors are the target sites where the primary active thyroid hormone, T3, binds, triggering its actions to drive cellular metabolism and maintain body temperature. Yet there is no credible scientific evidence that rT3 even enters the nucleus of the cell. While rT3 does not bind to, and has no known transcriptional activity at, the thyroid receptor, it does have potent non-genomic activity, mediated by binding to a specific thyroid receptor in the cytoplasm, as an initiator of actin polymerization in astrocytes in the brain [8][9]. ...
...
There appears to be little clinical justification for routine testing of rT3 for thyroid function assessment [14]. ...
 
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