Long Covid: a report from china

Logo of frontendo

Euthyroid Sick Syndrome (Functional Hypothyroidism) in Patients With COVID-19

Runmei Zou,1,†Chenfang Wu,2,†Siye Zhang,2Guyi Wang,2Quan Zhang,3Bo Yu,2Ying Wu,2Haiyun Dong,2Guobao Wu,2Shangjie Wu,4 and Yanjun Zhong2,* https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7575767/ Published online 2020 Oct 7. doi: 10.3389/fendo.2020.566439PMCID: PMC7575767PMID: 33117282

“Euthyroid Sick Syndrome” (ESS) is Functional Hypothyroidism (see my post on thyroid). It is the physiologic adaptation and pathologic response to stress, particularly to the stress of acute disease. It can be defined as a state in which T3 and T4 are low, without increased TSH.
In the pathophysiological process of ESS, type III deiodinase is activated and type I is suppressed, so there is preferential conversion of T4 to rT3 instead of T3 (9), conversion of free T3 to (inactive) T2 and reduced importation of T4 into the cells.
In addition, there is increased binding of thyroid hormone to plasma protein.
For these reasons, Free T3 plummets.
ESS occurs in infection, trauma, myocardial infarction, malignancy and virtually all other severe diseases (10). Previous studies have suggested that low levels of free T3 (FT3) are associated with severe disease and poor prognosis in critical illness (11, 12).
For example, a study consisting of 503 patients diagnosed with community-acquired pneumonia reported that ESS is an independent risk factor for mortality (19).
Also, in a previous study of 48 SARS patients, 93.7% patients had low T3 (8), high ESR and procalcitonin, but lower lymphocyte count than those without ESS (in this study, Cortisol and rT3 levels unknown).

Herein, Zou et al report studying 149 COVID-19 patients: 41 (27.52%) had ESS (9). 14 of the 41 (34.15%) were male and 65.85, female.
The median age was 58 (IQR: 50–66Yr).
The COVID-19 patients with ESS had stronger inflammatory responses, with higher CRP, ESR and Procalcitonin, but lower lymphocyte count than those without ESS (the levels of Cortisol and rT3 were unknown). ESS patients had more fever [39 (95.12%)], fatigue [18 (43.90%)], cough [36 (87.80%)], shortness of breath [25 (60.98%)], expectoration [20 (48.78%)], and anorexia [21 (51.22%)] than patients without ESS. Hypertension [10 (24.39%)] and diabetes [7 (17.07%)] were the common comorbidities.

Patients with ESS had significantly lower T4 and free T4 (FT4) than non-ESS patients, but the TSH did not differ.

WHY IS THIS IMPORTANT?
The authors have neatly proven that over 25% of their Covid patients had ESS (Functional Hypothyroidism, “FH”) but evidently they are not familiar with the condition and have not made the obvious connection: the symptoms of “long covid” and ESS/FH are indistinguishable.

In my opinion (please remember that since I am no longer licensed, my opinion does not constitute medical advice or instruction), long covid can be equated with ESS/FH and as such, can be expected to respond to administration of oral Triiodothyronine (dose supervised by a physician and titrated according to response of serum T3, rT3, ESR, CRP & TSH), along with support of other hormones, vitamins and minerals, as necessary.

  • References: (NOTE that these references are from the paper by Zou et al. They are not the product of my research).

1. Lu H, Stratton CW, Tang YW. Outbreak of pneumonia of unknown etiology in Wuhan, China: The mystery and the miracle. J Med Virol (2020) 92:401–2. 10.1002/jmv.25678 [PMC free article] [PubMed] [CrossRef] [Google Scholar] 2. Hui DS, Azhar EI, Madani TA, Ntoumi F, Kock R, Dar O, et al. The continuing 2019-nCoV epidemic threat of novel coronaviruses to global health – The latest 2019 novel coronavirus outbreak in Wuhan. China Int J Infect Dis (2020) 91:264–6. 10.1016/j.ijid.2020.01.009 [PMC free article] [PubMed] [CrossRef] [Google Scholar]
3. Huang C, Wang Y, Li X, Ren L, Zhao J, Hu Y, et al. Clinical features of patients infected with 2019 novel coronavirus in Wuhan. China Lancet (2020) 395:497–506. 10.1016/S0140-6736(20)30183-5 [PMC free article] [PubMed] [CrossRef] [Google Scholar]
4. World Health Organization Novel Coronavirus (2019-nCoV) situation reports. Available at: https://www.who.int/emergencies/diseases/novel-coronavirus-2019/situation-reports/ (Accessed Assessed on Augest 28th, 2020). 5. Coronaviridae Study Group of the International Committee on Taxonomy of The species Severe acute respiratory syndrome-related coronavirus: classifying 2019-nCoV and naming it SARS-CoV-2. Nat Microbiol (2020):536–44,0.1038/s41564-020-0695-z [PMC free article] [PubMed] [CrossRef] [Google Scholar]
6. Wadman M, Couzin-Frankel J, Kaiser J, Matacic C. How does coronavirus kill? Clinicians trace a ferocious rampage through the body, from brain to toes. Science (2020). 10.1126/science.abc3208 [CrossRef]
7. Zhu N, Zhang D, Wang W, Li X, Yang B, Song J, et al. A Novel Coronavirus from Patients with Pneumonia in China, 2019. N Engl J Med (2020) 382:727–33. 10.1056/NEJMoa2001017 [PMC free article] [PubMed] [CrossRef] [Google Scholar]
8. Wang W, Ye Y, Yao H, Li H, Sun L, Wang A, et al. Evaluation and observation of serum thyroid hormone and parathyroid hormone in patients with severe acute respiratory syndrome. J Chin Antituberculous Assoc (2003) 25:232–4. [Google Scholar] 9. Boelen A, Kwakkel J, Fliers E. Beyond low plasma T3: local thyroid hormone metabolism during inflammation and infection. Endocr Rev (2011) 32:670–93. 10.1210/er.2011-0007 [PubMed] [CrossRef] [Google Scholar]
10. Lee S, Farwell AP. Euthyroid Sick Syndrome. Compr Physiol (2016) 6:1071–80. 10.1002/cphy.c150017 [PubMed] [CrossRef] [Google Scholar]
11. Scoscia E, Baglioni S, Eslami A, Iervasi G, Monti S, Todisco T. Low triiodothyronine (T3) state: a predictor of outcome in respiratory failure? Results of a clinical pilot study. Eur J Endocrinol (2004) 151:557–60. 10.1530/eje.0.1510557 [PubMed] [CrossRef] [Google Scholar]
12. Bertoli A, Valentini A, Cianfarani MA, Gasbarra E, Tarantino U, Federici M. Low FT3: a possible marker of frailty in the elderly. Clin Interventions Aging (2017) 12:335–41. 10.2147/CIA.S125934 [PMC free article] [PubMed] [CrossRef] [Google Scholar]

BACTEROIDES: A Species of gut bacteria LINKED TO enhanced cognition and language skills in infant boys

From https://doi.org/10.1080/19490976.2021.1930875, Published online16 Jun 2021

This study found that boys with Bacteroides germs in their bowel had enhanced brain development. This University of Alberta-led research followed more than 400 infants from the “CHILD” Cohort Study in Edmonton.

Boys with a gut bacterial composition high in the Bacteroidetes germs at one year of age were found to have more advanced cognition and language skills one year later. The finding was specific to male children.

Dr. Anita Kozyrskyj, professor of pediatrics at the U of A and principal investigator of the SyMBIOTA (Synergy in Microbiota) laboratory, with associate professor Piush Mandhane and their research team, studied bacteria from the infants and identified three groups exhibiting similar dominant bacterial clusters. They then evaluated the infants and found that only male infants with Bacteroidetes-dominant bacteria showed enhanced neurodevelopment.  “We know that Female children score higher (at early ages), especially in cognition and language,” said Dr. Kozyrskyj,  “but when it comes to gut microbial composition, it was the male infants where we saw this obvious connection between the Bacteroidetes and the improved scores. The differences between male and female gut microbiota are very subtle, but girls are more likely to have more Bacteroidetes. So perhaps most girls have a sufficient number of Bacteroidetes and that’s why they have improved scores over boys”.

The research replicates similar findings from a U.S. study.

According to Dr. Kozyrskyj, Bacteroidetes produce metabolites called sphingolipids, which we need for brain growth. “It makes sense that if you have more of these microbes and they produce more sphingolipids, then you should see some improvement in terms of the formation of neuron connections in our brain and improved scores in cognition and language,” she said.

According to Dr. Kozyrskyj, caesarean birth can significantly deplete Bacteroidetes. Also, the infant’s gut microbiota Factors improve if they are breasted, have a high-fibre diet, live with a dog and are exposed to nature and green spaces.

While the findings don’t necessarily mean that children with a lower proportion of Bacteroidetes will remain behind their peers in later childhood or adulthood, the researchers believe that the study offers a way to potentially identify children at risk of neurodevelopmental disorders.

xxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxx

NOW, THIS IS FOR THE NERDS:

If you must have every last detail about Bacteroides, see/visit a paper entitled “Bacteroides: the good, the bad and the nitty-gritty”, by Hannah M Wexler. This is a well-written, amazingly detailed treatise on Bacteroides which will give you answers to your every question on the subject.

You can access the phenomenal Ms. Hannah Wexler’s paper on Bacteroides in: Clin Microbiol Rev, 2007 Oct:20 (4): Pages 593-621. doi: 10.1128/CMR.00008-07,  At ………………  https://pubmed.ncbi.nlm.nih.gov/17934076/

No more “Doctor” Harrys (at least, not in my family)

My great-grandfather, Philip Nathan “Archippus” Harry, MD, may his soul rest in peace, must be dismayed that the family tradition which he started is no more: two of his sons were medical specialists (an Ophthalmologist and an Otorhinolaryngologist) in England, one grandson (my father) was a surgeon in Jamaica and my brother and I worked in Toronto, he as a family psychotherapist and I as a urologist: none of our ten (in total) children has elected to study medicine. My brother retired in 2020 and I, now 17 years past my “best before date”, will be retiring on the first of July.

I have had an interesting, enjoyable and fulfilling career, which I would have liked to continue through age 95, but prudence dictates otherwise: so goodbye, and thanks to all of you for your faithfulness and your many kind words, over the past 57 years.

I hope that your new functional medicine practitioners perform to your satisfaction and I hope that this website, including my “blog” will keep you updated and assist your efforts to take an active part in your healthcare.

I will continue this blog as long as I am able: I hope that you will enjoy it as much as I do.

Sincerely, Gervais A. Harry.

Blood groups A and B are Covid19 risk factors

2021-05-13, from “Blood Reviews“, https://www.sciencedirect.com/science/article/pii/S0268960X20301351: “Systematic review and meta-analysis indicated that blood groups A and B may be risk factors for COVID-19, whereas the blood group O appears to be protective.”

CONCUSSION RISK, IN SOCCER

2021-05-08: Teenage girls face almost double the risk of concussion playing soccer, compared with teenage boys (risk ratio 1.88, 95% confidence interval 1.69 to 2.09, P<0.001)…. Reported by Gareth Iacobucci.

COMMENT: This report is based on a good study and is to be believed, but it raises a question: what’s the difference between boys and girls?

The two explanations I can think of are: (1) Concussion in soccer is due mostly to blows to the head sustained in “heading” the ball …. when something hits the head, the blow is transmitted to the brain under the point of impact, causing the brain to move. The moving brain then hits the opposite side of the skull with equal force (“contrecoup”) and each time the ball is “headed” the brain gets two “hits”. So, since males have stronger neck muscles, the sudden movement of the head in heading, and the “front and back” impacts sustained by the brain, are less. (2) If the player moves the head to strike the ball actively, the force of the “hit” is greater, but the brain-jiggling jerk of the skull is less. Maybe girls head passively, allowing the ball to hit the head without tensing the neck muscles. If so, the jerking of the skull must be greater and the back-and-forth “jiggling” of the brain much more pronounced.

NOTE: The brain is a jelly, with connecting nerves running through it which are made of slightly stronger, but really fragile, jelly. Rapid jiggling causes stretching and tearing of the nerves every time the skull receives a shock. Therefore concussions are cumulative: repeated small injuries add up to real problems.

POSSIBLE SOLUTIONS: (1) Change the rules, to outlaw heading, or (2) Teach girls active heading and (3) Include neck-strengthening exercises in training programs.

Dr. Harry.

DESSICATED THYROID RECALL

WEBMD HEALTH NEWS

Some Thyroid Drugs Recalled Over Reduced Potency

By Nancy Melville

May 04, 2021 — In its third voluntary recall in the past year, Acella Pharmaceuticals has announced a nationwide recall of specific lots of its popular thyroid treatment NP Thyroid tablets USP, this time after routine testing found the pills to be less potent than what the label says.

ADVERTISEMENT

Specifically, the affected lots were found to contain less than 90% of the drug’s two labeled ingredients to treat hypothyroidism: liothyronine (LT3) and/or levothyroxine (LT4).
The recalled lots include 15 mg, 30 mg, 60 mg, 90 mg and 120 mg pills packed in 100-count and 7-count bottles.
See the full list of recalled drugs on the FDA website.
There have been 43 reports of serious problems in patients that could be related to the recall.
Signs you may have one of the recalled drugs include the common signs of hypothyroidism, such as fatigue, increased sensitivity to cold, constipation, dry skin, puffy face, hair loss, slow heart rate, depression, swelling of the thyroid gland and/or unexplained weight gain or difficulty losing weight, Acella reports.

“There is reasonable risk of serious injury in newborn infants or pregnant women with hypothyroidism including early miscarriage, fetal hyperthyroidism, and/or impairments to fetal neural and skeletal development,” the company cautions in the recall statement.
Acella adds that toxic heart problems related to hyperthyroidism, including chest pain, heart palpitations or irregular heartbeat may happen in elderly patients and patients with heart disease.
While Acella is working to stop distribution of the recalled products, patients who are currently taking these medications should keep taking them and contact their doctor for further guidance.
In November, the same drugs were recalled for having lower-than-specified potency.
And in May 2020, the company recalled 13 lots of the tablets that were overly potent, with FDA testing showing some tablets contained up to 115% of the labeled amount of LT3.
If you have questions about the recall, email Acella Pharmaceuticals at recall@acellapharma.com or call 888-424-4341, Monday through Friday from 8 a.m. to 5 p.m. ET.

WebMD Health News from MDedge

ON THE SUBJECT OF FIBROMYALGIA:

ON THE SUBJECT OF FIBROMYALGIA:

The online literature is replete with both scientific and lay articles on fibromyalgia, the cause of which has not been elucidated and treatment for which is as yet non-existent.

Perhaps my experience and an interpretation of my history may be of benefit to some sufferers: hereunder the story.

CASE HISTORY

I had the childhood good fortune to be blessed with an extraordinarily stable, supportive, appreciative family and my innate self-confidence and self-reliance, combined with very mild autism spectrum (? slight Asperger’s) attributes, made me subjectively, extremely steady, stress resistant and consciously tranquil.

However I am subject to mild future-oriented apprehension (?fear?), first noted by my mother when I was age 6 (she frequently noticed me clenching my hands during sleep).

1974: I was fit and healthy. I qualified as a Urologic surgeon in April and on the 30th of June, left for Montego Bay, Jamaica, to be the sole urologist for a population of approximately 600,000 (very high professional stress).

1976: Professionally, life was great; but living in Montego Bay was untenable due to socio-economic and political factors. I returned to Canada on 1st July.

1976: I began work as a Urologist in September. Starting a freelance practice in the inner city and competing with 25 urologists at eight teaching hospitals and two other urologists at  my own facility, was extremely stressful.

1979: My legs lost hair and my kneecaps developed tendinitis.

1981: The tendinitis continued, with the beginnings of calcium deposition in the patellar tendons. I had severe constipation for the first time, with intermittent bouts of IBS. I gained weight, increasing from 145 pounds to 170 in 1990 and a maximum of 193 pounds by 2001.

1982: I started to have constant hives: complete laboratory testing was normal (HSCRP was not done). Bone growths in my Kneecaps grew larger, then my “sitbones” developed painful, very tender tendinitis. Heberden’s nodes developed in both hands.

1994: Kneecap and sitbone pain and tenderness (severe, spreading pain at the slightest touch) continued. My professional practice was good, but I had my prostate removed for cancer and couldn’t work for 3 months.

1997: Michael Harris closed my 3 hospitals: I was “fired”! I accepted a professorship at Tabuk hospital in Saudi Arabia.

1998: I developed fibromyalgia, which maximised by 2004 and then persisted.

2001: Weighing 193 pounds, I developed mild diabetes, which went away after weight loss to 176 pounds.

2006: I began taking DHEA, which helped the fibromyalgia, reduced the tendinitis pains, started to shrink the bony kneecap lumps and made the Heberden’s nodes shrink slowly.

2015: I self-diagnosed functional hypothyroidism (FH) and tried desiccated thyroid: it made the FH worse, so I stopped it (see “the thyroid, T3 and rT3 dominance”).

2016: My IBS became constant. Colonoscopies showed multiple diverticula and mild colitis.

2017: In January I began to treat my FH with T3. The fibromyalgia improved a bit, but In April I developed Polymyalgia rheumatica. (severe shoulder pain). A prescription of Prednisone “cured” the polymyalgia, but the IBS got worse and blood tests showed that “HS CRP”**** was up to 134 (normal = less than 1.0). In May a CAT scan showed an abscess of the colon. Treatment  with antibiotics, until October, was unsuccessful.

2018: My sigmoid colon was removed in February and within one week, my IBS symptoms disappeared, the hives went away and the fibromyalgia pain stopped (this, after 20 years!).

2021: Since the surgery in February, 2018 I have remained well. Heberden’s nodes no longer exist. the bony Patellar tendon lumps are half their previous size. I continue taking DHEA, Progesterone, Melatonin and T3. I also take CoQ 10 (200 mg), I3C (200 mg), Mg citrate (150 mg), NAC (900 mg), MTHF (2 mg), Vit.D (5000 iu). Now, retrospective analysis has led to the conclusion that although I was not consciously aware of stress between age 20 and age 75, constant, subconsciously perceived stress (from medical school, marriage at age 23 while still a student, then internship, then managing a remote, 60 bed country hospital for a population of 4000 with no assistant and no specialists to refer to, then moving to Canada for a 5-year residency in Urology, then 2 years in Montego Bay as the only urologist for 600,000 people, then relocating to Toronto to start a solo, unsupported urology practice in the inner city core) had eventually led to functional hypothyroidism*, starting a cascade of conditions for which the eventual cure was (A) NeuroHormone support, (B) Correction of Functional Hypothyroidism and (C) surgical removal of the potentially lethal end result-of the “cascade”.

OPINION I can’t say categorically that fibromyalgia is usually due to IL-6, which the bowel makes to heal diverticulitis, but in my case, it was. The thought process is as follows:

  • Stress caused Functional Hypothyroidism.
  • (Functional) Hypothyroidism caused constipation and eventually, weight gain.
  • Constipation caused increased pressure in the colon, producing diverticulosis.
  • Diverticular inflammation caused IBS and secretion of IL-6, which caused patellar tendinitis with bone formation in the kneecap tendons and (beginning in1982) muscle aches, especially where Gluteus Maximus attaches to the “sitbones”.
  • Stress from being “fired” by Michael Harris and relocating to a teaching position in Saudi Arabia in 1997 caused subconscious PTSD and worse functional hypothyroidism, which caused weight gain and borderline diabetes.
  • By 1998, the diabetes facilitated inflammation of the diverticula (“diverticulitis”).
  • Diverticulitis damaged the bowel lining, which increased production of IL-6 so as to heal itself.
  • The increased level of IL-6 caused increased muscle inflammation, presenting as fibromyalgia.
  • Prescription of DHEA in 2006 produced slight improvement of the fibromyalgia.
  • Stress from “semiretirement” in 2014 increased FH, recurrence of constipation/IBS/diverticulitis.
  • Massive elevation of IL-6 from one diverticulum which had become badly infected led to polymyalgia rheumatica.
  • Prednisone, prescribed for polymyalgia rheumatica, restarted the diabetes.
  • Diabetes caused the inflamed diverticulum to form a huge, closed abscess.
  • Complete removal of the diverticulitis-laden bowel resulted in complete cure of the IBS, hives and fibromyalgia.
  • NOTE: the Heberden’s nodes were incidental, caused by age-relatedDHEA hormone deficiency. They had nothing to do with IL6, Thyroid or Diabetes.

 *   ”Functional hypothyroidism” is a condition in which “T3”, the active thyroid hormone, stops working. It can coexist with true hypothyroidism. See the page titled “THYROID”.

**  IL-6 is a “cytokine”, which promotes healing of damage to the bowel lining but produces inflammation elsewhere, particularly in muscles. Cortisone/Prednisone and other “Glucocorticoids” block it 100%, resulting in improvement of muscle pain, but failure of the bowel damage to heal. There are many other cytokines, some anti-inflammatory and some ruinously pro-inflammatory: see Wikipedia (blog follows later).

*** “Perceived stress” is stress which is subconsciously perceived by the brain, even if the individual claims to be stress-free.   

       “Subjective stress” is stress which is consciously noted and “felt”, and can be described, by the individual.

       “Objective stress” is an evaluative term to denote stress to the individual, as observed by others.

**** HS CRP is made in the liver, in response to rising IL6.

***** ”Steroidopenia” is deficiency of the neurosteroid hormones, DHEA, Testosterone, Oestrogen and Progesterone.

REGARDING FUNCTIONAL HYPOTHYROIDISM Functional Hypothyroidism is a state in which the thyroid “#4″ hormone, T4, produced by a normally functioning thyroid gland, is converted by the body into a “twisted” form of thyroid 3 hormone called Reverse T3 (rT3), which does not work. In this situation, symptoms of thyroid 3 hormone deficiency (see list, below) develop even though routine thyroid hormone testing (TSH, T4, T3) is normal. Functional Hypothyroidism cannot be diagnosed by family MDs because they do not test for rT3 …….. OHIP won’t pay for the test either and the lab will charge you $50.00.

See “reverse T3 dominance” on the THYROID page of this website.

The effects of functional hypothyroidism are the same as those of true hypothyroidism: see “the symptoms, signs, diagnosis and treatment of hypothyroidism” on the THYROID page.

Twisted thyroid 3 is produced when the brain perceives high stress: see “the thyroid, T3 and reverse T3 dominance”.

FH is easily treated with Triiodothyronine (thyroid hormone #3, or “T3”): see “treating Functional Hypothyroidism”.

Over-treating functional hypothyroidism can produce hyperthyroidism (too much thyroid 3 hormone): this is easily diagnosed by testing 2 weeks after starting the prescription and resolves as soon as the dose of T3 is reduced:

see “treating functional hypothyroidism”.

Stress-induced functional hypothyroidism (“FH”), which may be superimposed on true hypothyroidism, is endemic in our population and is a factor in all severe illness, either as a partial cause of the illness or as a result of it.

My history is a good example – it is easily explained on the basis of stress-induced FH, which began in 1979 but was not diagnosed until 2015.

Since my bowel problem began because of functional hypothyroidism, early diagnosis of FH, with appropriate therapy, might have prevented the entire scenario.

Early (3rd or 4th decade) assessment of hormonal balance, with appropriate supplementation, might have prevented the development of FH by reducing the level of “perceived” stress**.

Routine surveillance for steroidopenia***** and functional hypothyroidism should begin as early as possible, ideally at age 15, with a view to correction of hormonal imbalances and therapy for functional hypothyroidism ASAP.

PROPOSAL FOR ASSESSMENT OF AND SUPPORT FOR FIBROMYALGIA, SPECIFICALLY

Once the fibromyalgia diagnosis has been made, or even suggested, lab, Ultrasound and CAT/MRI investigation should look for inflammations: possible causes of elevated CRP and other cytokines. The list should include a blood count with ESR, urine examination with culture for germs, kidney and liver function tests, cholesterol and HS CRP, stool tests for blood, worms and infections, vitamins B12, B6, B9 and D, hormone check (DHEA, free testosterone, oestradiol, oestrone, progesterone), thyroid (TSH, T4, T3, rT3 and thyroid antibodies) and homocysteine. Men over 40 should do a PSA test and if available, the new blood test for Alzheimer’s should be requested. Correction of problems demonstrated by this testing, plus hormonal balancing, should be instituted in addition to fibromyalgia treatments.

Just when you thought that family doctors would never learn about prescribing T3:

Jacqueline Jonklaas, Professor in the endocrinology division at Georgetown University, has submitted a paper entitled “Evidence-Based Use of Levothyroxine/Liothyronine Combinations in TreatingHypothyroidism”

Below are excerpts from a (2nd March, 2021) report in Medscape Medical News:

“Numerous trials have been conducted on short-acting liothyronine (LT3) in combination with the standard therapy of levothyroxine (LT4). However, the experts agreed that shortcomings in the existing studies and mounting unanswered questions need to be addressed, Jacqueline Jonklaas, MD, PhD, told Medscape Medical News“……………

“Patient-reported outcomes were acknowledged as essential in the full picture of understanding treatment efficacy, and the experts agreed that an emphasis on those outcomes will be important in any future trials of combination therapy.”

“Among the key topics agreed upon is the need to evaluate a sustained-release T3 preparation. Such a preparation could overcome concern of the dissipation of circulating T3 that occurs with oral tablet formulations, which fail to achieve the relatively stable levels seen in normal individuals, Jonklaas noted.”

“There was unanimous agreement that when and if a sustained-release T3 preparation became available and had undergone preliminary testing, new trials with such a preparation were definitely warranted,” she said. Preliminary testing of a new product that potentially provides sustained release of T3 has recently started.

WHAT THIS MEANS, TO YOU AND ME:

THIS MEANS that doctors have finally begun to listen what patients have been saying for the past many years: the accepted treatment of hypothyroidism using Ltroxin and Synthroid doesn’t work and the time has come to prescribe T3, or a combination of T3 and T4, instead.

So in a couple of years, the use of slow-release T3 will be accepted, the misery of millions who have been treated with T4 alone will come to an end and “the system” will authorise prescription of slow-release T3 as a “covered” medication.

WHAT IS A HORMONE, AND WHY DO WE NEED THEM?

An endocrine hormone is a molecule produced by a hormone-secreting gland and carried by the blood to another organ, whose behavior it controls. Generally, the Hormone plugs into a specific receptor protein in the target cell, changing the shape of the receptor protein and thereby, producing a change in cell function.

Hormones are used to communicate between organs and tissues to regulate physiological and behavioral activities, such as digestion, metabolism, respiration, tissue function, sleep, excretion, lactation, stress, growth and development, movement, reproduction and mood.

It is also possible for a cell to produce a hormone to control activity within itself [an “Intracrine” hormone] or to control nearby cells in the same organ [a “paracrine” hormone].

There are many kinds of hormone molecules: eicosanoids, steroids, amino acid derivatives, peptides, proteins etc.

Some are soluble in water, while some only dissolve in oils and fats (lipids). The lipid-soluble ones need special transport proteins in the blood, to transport them from their gland of origin, to the target organ.

Hormones pack a powerful punch, in terms of their effect on the body. Therefore they need to be “balanced”: produced in exactly the right amounts, at the right time, to keep the target organs running smoothly and to keep the body as a whole, “in tune”. This is achieved by a delicate; but effective “feedback system” in which a chemical [often, another hormone] produced by the target cell goes back to the hormone producing gland, which can tell how much target hormone is present in the blood and modifies its production accordingly.

They are also produced in a “diurnal rhythm”, with maximum production at a particular time of day. Each hormone has its own rhythm. For example thyroid 3 hormone is boosted at 4 AM and testosterone at 8 AM.

The brain controls hormone production and the system is rather like an amplified orchestra:

[1] The Pineal gland is the (diurnal) timer, to tell the system when to sleep and when to play.

[2] The Hypothalamus detects input signals from the hormonal glands, skin nerves, blood chemicals, intestines, eyes, ears and emotions (in fact, the whole body), and balances the output of control hormones by the Pituitary.

[3] The Pituitary gland, like a conductor, tells the individual players when and how forcefully, to play their part.

If all is in balance, the individual player does just the right amount of work and the system is in tune.

Outside of the brain, there are many players:

Major “generalist” glands like the skin, the thyroid, the parathyroids, the pancreas, the intestine, the adrenals and the gonads (ovaries in the female and testicles in the male) produce hormones which affect the entire body,

Specialist” hormone producers like the kidneys, stomach, bowel, placenta and the fat make hormones which are included in the Hypothalamus’ calculations, but also act directly on other specific glands or tissues.

Micro factories in all the cells process Pregnenolone, DHEA, Levothyroxine (“thyroid #4 hormone”, or “T4”), Cortisol and other “generalist” hormones into specific molecules for that cell’s own maintenance and repair.

WHY DO WE NEED THEM?

Every cell in your body, from your skin and hair, to your brain and all your other parts, dances to the beat of your hormones and can only function optimally when they are “in tune”.

Hormonal imbalance can be responsible for physical dysfunction, including obesity, for cognitive dysfunction including “fuzzy thinking”, for psychological dysfunction, including anxiety, panic attacks and depression and perhaps for Alzheimer’s disease.

Therefore in a significant proportion of cases, hormonal “restoration” or “rebalancing” will return the individual to stable, normal function.

G. A. Harry, MD.

REFERENCES, FOR “WHAT IS A HORMONE AND WHY DO WE NEED THEM?”:

1: DEFINITION – Wikipedia:https://en.wikipedia.org/wiki/Hormone

2: RECEPTORS – Wikipedia:https://en.wikipedia.org/wiki/Receptor_(biochemistry)

3: TRANSPORT PROTEINS – Wikipedia:https://en.wikipedia.org/wiki/Transport_protein

4: PINEAL GLAND – Britannica:https://www.britannica.com/science/pineal-gland

5: HYPOTHALAMUS – Britannica:https://www.britannica.com/science/hypothalamus

6: PITUITARY – Merck:https://www.merckmanuals.com/en-ca/home/hormonal-and-metabolic-disorders/pituitary-gland-disorders/overview-of-the-pituitary-gland

7: PUBMED:

[A]: 17 BETA HYDROXY STEROID DEHYDROGENASES https://www.ncbi.nlm.nih.gov/pubmed/11091120

[B] INTRACRINOLOGY (Prof Fernand Labrie) https://www.ncbi.nlm.nih.gov/pubmed/10915214

8: THYROID GLAND FUNCTION – https://mcb.berkeley.edu/courses/mcb135e/thyroid.html

9: REGARDING AGING – https://www.nature.com/articles/d41586-018-05582-3

10: EVERYTHING YOU WANTED TO KNOW ABOUT THE PINEAL GLAND – https://www.globalhealingcenter.com/natural-health/everything-you-wanted-to-know-about-the-pineal-gland/#1

https://en.wikipedia.org/wiki/Pineal_gland

G. A. Harry, MD [Retired]

DHEA

The letters “DHEA” are an acronym for DEHYDROEPIANDROSTERONE: this is the hormone which is produced in greatest quantity by the youthful human body. In smaller animals, the hormone is produced entirely in the brain and blood levels tend to be very low. The brains of humans and the Primates also make DHEA, but in addition the adrenal glands process cholesterol into Pregnenolone, from which DHEA is made in such large amounts in youth, that weight-for-weight, it exceeds the aggregate of all the other hormones.
DHEA levels are high at birth because the mother produces large amounts during pregnancy and the hormone crosses the placenta to the baby. Levels fall rapidly after birth and remain low until age 8 – 13 or so, at which point both males and females begin to maximise DHEA production.

DHEA circulates in the blood stream and is used by all cells in the body, individually, to produce such hormones and hormone byproducts as each particular cell needs for efficient function: Intracellular hormonogenesis has been termed “Intracrine” by Dr. Fernand Labrie, Professor of Endocrinology at the University of Laval.

The DHEA molecule is modified by a family of “3 beta hydroxy steroid dehydrogenase” enzymes, producing dozens of different “micro-hormones” and from those, further modifications are made, so that within each cell, a specialised hormone mix is produced, which facilitates the function of that particular cell type: this is part of the reason why the ends of your fingers make fingernails, while special cells in your bones make blood, et cetera.

Beginning at age 25-30 in females and 35 (or earlier) in males, production falls by approximately 1-3% per annum, so that by age 80 the blood contains mainly intracerebrally-produced DHEA, with hardly any output by the Adrenals. Thus the blood level in old age is 10 % or less of that at age 20.

As with everything else in nature, there is a “spread”, Bell-curve-wise, of DHEA levels in youth. The disparity between the highest and lowest rate of synthesis is maintained throughout life, so that those with the lowest production early on tend towards zero production in old age. At the left end of the bell curve, there is a small proportion of the population whose DHEA production is suboptimal even in the teenage years and “80-year-old” serum concentrations can at times, be seen in the second decade.

Thus a deficiency in production of DHEA can be found at any age and can lead to inefficiency of hormonal function in any part [or many parts] of the body, including the central nervous system and the “immune system”. Because of this, the clinical manifestations of DHEA deficiency vary from person to person, depending on which of an individual’s organs happens to be most sensitive to reduction in its availability. The symptoms are therefore highly variable. The commonest problems in both sexes, however are those which result from Testosterone deficiency; this is not a surprising finding, given the multiplicity of functions which that hormone subserves.

The subject of DHEA is a bone of contention in the medical community; there are 3 “teams”: very enthusiastic lay people who think that everybody should supplement their DHEA so as to slow down aging, researchers who are mostly “pro” and a group of naysayers and doomsayers, whose objections are mainly of the “What if”, “Perhaps” and “We don’t know, so we can’t recommend it” variety.

In view of this it is important to note that in spite of the easy, “OTC” availability of DHEA in the USA, no life-threatening complication has ensued: as Dr. Fernand Labrie, Professor of Endocrinology at Laval U. and an acknowledged expert in the field avers, no serious adverse event related to DHEA has ever been reported in the world literature (thousands of subjects exposed) or in the monitoring of adverse events by the FDA (millions of subjects exposed)”.

The bottom line of all this is that without a good supply of DHEA, something is bound to go haywire and the corollary is, restoring your DHEA and maintaining it at youthful levels promotes ongoing normal function in all parts of the body, not just in those obvious functions which depend on testosterone.

%d bloggers like this: