Skip to content

Tag: tpo

New chemical analysis showing important difference between NDT and T4-only!

I found this fascinating…and I think you will, too.

I got an email from Peter Guagliano, the owner of the website thyroid-s.com. And he directed me his latest post titled “Natural Desiccated Thyroid and Synthetic are NOT the same”. 

But this wasn’t the basic information that we all know i.e. comparing a single synthetic hormone to all five natural desiccated thyroid, which makes the latter wonderful.

Instead, it was about a bio-analytical chemist who decided to test synthetic T3 (Cynomel and Cynoplus) as well as the Thailand-made Natural Desiccated Thyroid (NDT) called Thyroid-S, by extracting each tablet with methanol, then diluting and injecting them on an LC/MS system–a sensitive instrument used to detect and identify compounds and molecules in a substance.

And what he discovered and reported is that the thyroid hormones of NDT are tightly bound with thyroglobulin, a large iodine-containing protein….whereas synthetics are bound by nothing. i.e. synthetic hormones are exposed; NDT hormones are protected (until they are released by your digestion).   The diagram on this blog post gives you a powerful visual of this reality, but specifically in comparing natural desiccated thyroid with synthetic T4-only. You will see the large mass of thyroglobulin on the left, each containing either T4, T3, T2, T1 or calcitonin within. Then the tiny synthetic hormone on the right, alone.

But is that bad NOT be bound by thyroglobulin??  Possibly yes in the opinion of Peter. As Peter explained:  “The [exposed] synthetics might be affected by stomach acids in different ways in different people.  Low acid, high acid, various digestive and pancreatic enzymes in varying amounts, bacteria/flora in the stomach and small intestine, all kinds of possibilities here which would vary by the person.”  And, he says, that can mean instability!

Peter continues:  “Perhaps the thyroglobulin in NDT (and completely missing in the synthetics) is absorbed, or necessary, or utilized, or forms other products during digestion that could affect blood levels of various substances, numerous carrier proteins for example, thereby affecting the results obtained.”  And he concludes:  “The NDT hormones are bound to thyroglobulin and not available for reaction or breakdown until after they first digested (from Janie: which saliva begins, by the way, even in your mouth).  This would be a more stable compound.”  His original post is here.

A side note about thyroglobulin and iodine:   The protein Thyroglobulin takes up a lot of space in your thyroid with the purpose of taking ahold of iodine and storing it to produce thyroid hormones. That purpose alone tells you how important it is to have healthy levels of the nutrient iodine. And each molecule of thyroglobulin has just over 100 sites where the iodine can take ahold along with the assistance of thyroid peroxidase (TPO) and hydrogen peroxide. When you are iodine deficient, it’s been noted that your thyroglobulin will increase, which is why you can see a bulge in front of your neck–also called a goiter. (Even taking too much iodine supplementation can cause this increase, which can block thyroid hormone production).

**Enjoy more scientifically technical information about thyroglobulin? Go here. 

**To read about the process of making porcine-derived NDT via thyroglobulin, go here. 

**To know more details about Natural Desiccated Thyroid–its history, the breakdown of the hormones, and how patients dose it, see Chapter 3 in the revised STTM book, here. 

**To read how T4-only is only a reverse mirror image of the real thing, read my blog post from May 10, 2012. 

Whether these findings are completely correct or not, patients simply know from ten years of experience that NDT has been giving them far better results than T4-only…and even those on T3-only who moved to NDT reported they liked the results even more. It’s all important patient-to-patient information.

23 replies

If you have Hashimoto’s, you may want to become aware of Hashimoto’s Encephalopathy

Screen Shot 2015-07-06 at 8.25.26 AM

Though this post first came up in 2010, it has been updated to the present day and time. 

*****************

I got an email from a sweet thyroid friend and advocate, Bev, aka Thyro-butterfly, whom I’ve known for several years. And Bev has had two relapsing and unnerving bouts with a condition that’s not common, and  under-diagnosed: Hashimoto’s Encephalopathy (HE).

She stated “I think everyone who has Hashimoto’s disease should know that this exists because the symptoms are so similar to severe neurological problems. And the treatment, though not curable, is relatively easy to do….”

What is Hashimoto’s Encephalopathy (HE)?

Hashimoto’s Encephalopathy is a rare neuroendocrine disorder which was termed and recognized in 1966 and has a strong connection to the autoimmune thyroid disease called Hashimotos–a form of Thyroiditis. i.e.  just as antibodies attack your thyroid, there are rare cases where it can attack and destroy your brain cells. Having a high thyroid peroxidase (TPO) antibodies lab result is common with Hashimoto’s Encephalopathy, and can accompany high anti-thyroglobulin antibodies, as well.

Researchers have also coined other names for this condition:

  • Steroid Responsive Encephalopathy Associated with Thyroiditis (SREAT)
  • Encephalopathy Associated with Autoimmune Thyroid Disease (EAATD)
  • Non-vasculitic Autoimmune Inflammatory Meningoencephalitis (NAIM)
  • Autoimmune Encephalopathy (AE)

The U.S. National Institutes of Health’s Office of Rare Diseases Research refers to it as Hashimoto’s Encephalitis.

Wikipedia states:

Up to 2005 there were almost 200 published case reports of this disease. Between 1990 and 2000, 43 cases were published. Since that time, research has expanded and numerous cases are being reported by scientists around the world, suggesting that this rare condition is likely to have been significantly undiagnosed in the past. Over 100 scientific articles on Hashimoto’s Encephalopathy were published between 2000 and 2013.[2]

What are symptoms that can make one suspicious of having HE?

Those with HE can share many symptoms, or can have unique symptoms from each other. They include:

  • tremors
  • seizures
  • jerking
  • language difficulty, whether speaking, writing or reading
  • confusion
  • limited attention span or concentration
  • poor memory and retention
  • dementia diagnosis
  • disorientation
  • restlessness
  • convulsions
  • symptoms similar to a stroke
  • poor coordination (walking, fingers, hands, etc)
  • partial right-sided paralysis
  • headaches
  • fatigue
  • sleep problems
  • psychosis
  • coma

Women are more prone to HE than men.

What tests might my doctor do to confirm this?

Studies underscore the need to first exclude “other toxic, metabolic and infectious causes of encephalopathy (disorder of the brain) with neuro-imaging and CSF examination”.  The latter is examining one’s cerebrospinal fluid. But when there are quite high levels of antithyroid antibodies like TPO (thyroid peroxidase), that alone can be a strong enough clue to diagnose Hashimoto’s Encephalopathy. High TPO antibodies can accompany high levels of thyroglobulin antibodies, as well.

What kind of doctor might help me the most?

Many of the published articles on HE have been done by Neurologists from the Mayo Clinic.  If you live in Arizona, Florida or Minnesota, here’s a list of Neurologists associated with Mayo: http://www.mayoclinic.org/departments-centers/neurology/sections/doctors/drc-20117077

Here’s a list of Neurologists by states in the US: http://www.healthgrades.com/neurology-directory

Around the world, you can click on the area you live, then see a list of Neurologists: http://www.wfneurology.org/member-societies

How is HE treated?

Luckily, treatment is fairly straightforward and dramatic against symptoms: steroid use, which is why it’s also termed “steroid-responsive encephalopathy associated with autoimmune thyroiditis (SREAT)”.

Says Elaine Moore in her article titled Hashimotos encephalopathy: A Treatable Form of Dementia:

Patients with SREAT show a good response to corticosteroids such as prednisone and related immunosuppressants because of the ability of these medications to reduce thyroid antibody production and reduce inflammation. Researchers in India report a case of SREAT that did not respond to corticosteroids but showed a very favorable response to plasma exchange, a technique used to remove circulating antibodies.” Doses of steroid can vary from individual to individual, but some do well on 4-6 mg cortisol for a few days. Others may need more.  Remission is the norm for most. You’ll have to watch for relapses. Since misdiagnosis is common, it’s important to talk to your doctor about this potential disorder, testing, and treatment if you have Hashi’s and symptoms similar to any of the above.

Wiki also states: Initial treatment is usually with oral prednisone (50—150 mg/day) or high dose IV methylprednisolone (1 g/day) for 3—7 days.

Thanks to Bev for bringing this issue back up.

 

 

70 replies