All PD patients in this study had intracellular hypothyroidism
Parkinson’s and the thyroid
A recent communiqué, delivered to my newsfeed, made reference to an interesting paper in Clin Exp Immunol, 2022 May 3;208(3):372–379. doi: 10.1093/cei/uxac044 . Entitled “Genetic correlation between thyroid hormones and Parkinson’s disease” and submitted by Jiyi Xu 1,2,#, Cheng Zhao 3,#, Ye Liu 4, Congjie Xu 5,6, Bin Qin 7, Hui Liang (PMCID: PMC9226140 PMID: 35511827).
The abstract reads as follows (paraphrased): “Parkinson’s disease (PD) is a progressive neurodegenerative disease, characterized by tremor, bradykinesia, myotonia, and non-motor symptoms. Clinically, degeneration of dopaminergic neurons in the substantia nigra, α-synuclein deposition, and Lewy body formation are characteristic pathological changes.
With the aging of society, the incidence of PD is increasing, but the pathogenesis is still unknown*. Dysfunction of the immune system is considered to be a critical cause of PD and has received increasing attention in the past decade.
An epidemiological study in Sweden (2023), involving more than 300 000 subjects, showed that patients with autoimmune diseases, such as amyotrophic lateral sclerosis, Graves’ Disease/Hyperthyroidism, Hashimoto’s Thyroiditis/hypothyroidism, multiple sclerosis, and rheumatoid myalgia, had an additional 33% risk of PD.”
* I would like to know whether stress, with low T3, close-to-zero DHEA and testosterone, plus deficiencies of pregnenolone, melatonin, magnesium, sulphur, Iodine, Selenium etc has anything to do with neurodegeneration, but no-one else seems to think in those terms!
A well written paper; but they entirely missed the significance of rT3!
The authors felt that the known correlation between thyroid function and PD was worth exploring and particularly, they wondered whether a genetic susceptibility to “autoimmune” disease might affect both the nervous system and thyroid function.
Therefore they undertook a study, aiming to answer two questions:
(1) whether there is a difference in thyroid hormone levels between PD and healthy controls and
(2) whether PD-related genes affect thyroid hormone levels.
They investigated a group of Parkinson’s Disease patients, comparing them with matched controls, with emphasis on the effect of 12 different SNP’s on the patient’s thyroid hormone.
Examining the genetic correlation between thyroid hormone function and PD, so as to analyse the effect of PD-risk genes on thyroid function, they found 12 “meaningful SNP’s” which could affect PD and thyroid function through an immune mechanism and discovered that thyroid function indices between PD and their control group were significantly different.
The study was very well designed and the comparisons between the 12 different groups were meticulously recorded, utilizing tables, of which I have copied one (below).
The object of this post
I have little interest in the authors’ prime concern, as to whether or not PD and thyroid disease are linked according to genetic characteristics. However I find their detailed analysis of the thyroid hormone parameters fascinating, revealing and hugely important to our understanding of hypothyroidism in general and Intracellular Hypothyroidism in particular: this is the first time that I have seen such a detailed list of thyroid tests, including reverse T3 (rT3), which is usually ignored!
I’m also interested in a segue, from Parkinson’s disease to myocardial failure: more on that, below; for now, let’s look at their tables:
Incredibly detailed thyroid function tables
Table 1 summarizes the characteristics and thyroid function indexes of participants. Comparing all eight indices of thyroid function (TT4, TT3, TSH, FT3, FT4, TPOAb, TGAb, and rT3) in the two groups, it was found that the levels of TT3, FT3, FT4, and TSH in the PD group were significantly lower than those in the control group, while rT3 was significantly higher than that in the control group.
Table 1:
– Note that normally, FT3 is between 2.3 & 4.2 Picograms per ml (3.2 to 6.2 Pmol per Litre. Thus the PD subjects actually did not have suppressed serum FT3 levels.
– However rT3, which should be less than 13 (see aT3/rT3 table, below table 1), ranged between 50 and 63 Ng/DL: this very high rT3 level,, common to all of the PD subjects under investigation, indicates that 100% of the patients had severe low T3 syndrome (defined as T3/RT 3 = <20).
This finding is repeated, with numbers very close to these, in all 13 of the tables presented in the article: I won’t bore you by copying the subsequent 12 tables, to this page!
The unusual FT3 (2.9 – 3.44 Pg/mL) and rT3 (48 – 63.28 Ng/DL) values are similar, in all 13 tables.
Note that Normal FT4 in adults is 0.8 to 1.8 ng/dL
No mention is made in the article, of iodine, selenium, magnesium or any other essential minerals, vitamins, amino acids or other nutrients and neither is mention made of hormones (DHEA, cortisol and the like), diet, lifestyle habits or exposure to heavy metals and other toxins, which might affect thyroid function will will will will.
The bottom line
There are two conclusions from table 1:
(1) The figures for all parameters, between patients and controls are not hugely different, including the reverse T3 levels, while the average rT3 among patients was 58, the average among the controls was 48: therefore the controls also had the Low T3 syndrome.– Please go to “hypothyroidism diagnosis” and read “Basic facts and the bottom line”– if the rT3 exceeds 20, T3/rT3 must be less than 20, unless the patient is hyperthyroid.
(2) The best free T3 level, 3.44 pg/mL, translates to 5.28 picomoles per litre and the worst, 3.01, is 4.62 pmol/L: both are normal, on the Ontario scale of 3.2 – 6.2. all the numbers you a T3/rT3 ratio of less than 10, indicating severe intracellular hypothyroidism.
These facts however do not change my conclusion, as stated below.
Subscribe to continue reading
Subscribe to get access to the rest of this post and other subscriber-only content.